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The HLA Region and Autoimmune Disease: Associations and Mechanisms of Action

M. Simmonds, S. Gough

Current Genomics · 2007

doi:10.2174/138920207783591690 (opens in a new tab)

Abstract

The HLA region encodes several molecules that play key roles in the immune system. Strong association between the HLA region and autoimmune disease (AID) has been established for over fifty years. Association of components of the HLA class II encoded HLA-DRB1-DQA1-DQB1 haplotype has been detected with several AIDs, including rheumatoid arthritis, type 1 diabetes and Graves' disease. Molecules encoded by this region play a key role in exogenous antigen presentation to CD4+ Th cells, indicating the importance of this pathway in AID initiation and progression. Although other components of the HLA class I and III regions have also been investigated for association with AID, apart from the association of HLA-B*27 with ankylosing spondylitis, it has been difficult to determine additional susceptibility loci independent of the strong linkage disequilibrium (LD) with the HLA class II genes. Recent advances in the statistical analysis of LD and the recruitment of large AID datasets have allowed investigation of the HLA class I and III regions to be re-visited. Association of the HLA class I region, independent of known HLA class II effects, has now been detected for several AIDs, including strong association of HLA-B with type 1 diabetes and HLA-C with multiple sclerosis and Graves' disease. These results provide further evidence of a possible role for bacterial or viral infection and CD8+ T cells in AID onset. The advances being made in determining the primary associations within the HLA region and AIDs will not only increase our understanding of the mechanisms behind disease pathogenesis but may also aid in the development of novel therapeutic targets in the future.

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Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 17, 2026. Paragraph numbers are ours, so an answer can point at one.

INTRODUCTION

Autoimmune diseases (AIDs) including type 1 diabetes (T1D), multiple sclerosis (MS), rheumatoid arthritis (RA), Graves’ disease (GD), ankylosing spondylitis (AS) and systemic lupus erythematosus (SLE) affect over 4% of the western population and involve the generation of autoantibodies against self antigen/s. In many cases lymphocytic infiltration of a target organ/s and autoimmune destruction is also observed. These diseases are often chronic and debilitating and, although treatments are available, many are inadequate providing the impetus for a greater understanding of the disease mechanisms and the development of novel therapeutic agents. Antigen presentation and T cell activation appear to be key to triggering an autoimmune response prompting investigation of many genes within this pathway for association with AID including several within the major histocompatibility complex (MHC).

The MHC, also known in humans as the human leukocyte antigen (HLA) region, encompasses 7.6Mb on chromosome 6p21 and is the most gene dense region within the human genome encoding 252 expressed loci including several key immune response genes. The region can be subdivided into the extended class I, classical class I, classical class III, classical class II and extended class II regions (Fig. 1) and contains the largest degree of polymorphism within the genome. It also exhibits the most dense linkage disequilibrium (LD), extending up to 540kb, which compares with distances of between 1-173kb seen in the rest of the genome. The extent of LD within the region has proved challenging when trying to tease out the exact location of etiological variants. Most studies have focussed on the role of HLA class II encoded HLA-DR and –DQ molecules, which present exogenous antigens for recognition by CD4+ T helper (Th) cells. Strong associations with almost all AIDs have been detected (see Table 1).

ASSOCIATION OF THE HLA CLASS II REGION WITH AID

Early experiments investigating association of HLA-DR and -DQ with AID in T1D indicated a strong association of the DRB1*03 and DRB1*04 alleles. A stronger association with the DQB1 locus alone was reported when an allele encoding aspartic acid (Asp) at position β57 of DQB1 was found to be associated with resistance to T1D, while an allele encoding a neutral residue, such as alanine (Ala) or serine (Ser) at position β57 conferred susceptibility. This molecule forms a critical residue in peptide binding pocket nine (P9) of the DQB1 binding pocket involved in antigen presentation and T cell receptor (TCR) interaction. It’s carboxylate group forms a salt bridge with arginine (Arg) at position α57 of the DQA1 chain that stabilizes the heterodimer between the DQA1 and DQB1 chains. The presence of Asp at this position could alter the stability of the molecule and/or antigen presenting repertoire, thus making the molecule more prone to binding autoreactive antigens. Although this may provide an interesting mechanism for association of the HLA class II region with T1D, further studies have demonstrated a potential role for other residues in DQB1 binding pocket P9 and DRB1 binding pockets P1 and P4 in disease susceptibility.

Association with RA is only seen at DRB1, with other associations with DQB1 almost certainly the result of LD with DRB1. Originally association was attributed to DRB1*04 but other associations have subsequently been reported. Work by Gregerson, et al, showed that association of DRB1 alleles (DRB1*0101, DRB1*0102, DRB1*0401, DRB1*0404, DRB1*0405, DRB1*0408, DRB1*1001 and DRB1*1402) was due to similarities within the DRB1 peptide domain at positions β70 through to β74, with these alleles containing similar sequences (QKRAA/QRRAA/RRRAA) termed the ‘shared epitope’. Amino acid changes within the shared epitope have been postulated to differentiate the predisposing alleles from the protective DRB1*0103, DRB1*07, DRB1*1201, DRB1*1301 and DRB1*1501 alleles. Recent work on the shared epitope has suggested a new model, whereby the shared epitope only consists of positions β72-β74, and rather than being essential for disease susceptibility, positions β70 and β71 have been proposed to modulate association. Further verification of this hypothesis, re-defining the shared epitope, is required.

Association of DRB1 position β74 of the share epitope is not unique to RA. In GD, comparison of the predisposing DRB1*03 and protective DRB1*07 molecules showed DRB1*03 containing a positively charged Arg at β74 and DRB1*07 containing a non-charged polar glutamine (Gln) at this position. Position β74 has also been shown to differentiate between the lower risk DRB1*0403 and *0406 T1D alleles, which contain a negatively charged glutamic acid (Glu), compared to the high risk DRB1*0401 allele which contain a non-charged polar Ala. Interestingly the DRB1*07 haplotype is also protective against T1D and RA. Amino acid (74 spans several binding environments involved in autoantigen binding/presentation and T cell antigen receptor docking and interaction, suggesting that changes within peptide and TCR binding could determine which amino acids are presented to the immune system.

Further work on DRB1 and DQB1 showed that there was LD between these molecules and, along with DQA1, they were found to form part of extended haplotypes DRB1*03-DQB1*02-DQA1*0501 (DR3) and DRB1*04-DQB1*0302-DQA1*0301 (DR4) associated with T1D. Overlap between HLA class II associations has been seen between AIDs, with DR3 also being associated with GD, SLE and HT, therefore, being termed the ‘autoimmunity haplotype’ (See Table 1 for list of common AID HLA class II associations). DR4 is also associated with other AIDs, including HT. Statistical modelling techniques, including logistic regression analysis, have been employed to determine which components of the DRB1-DQB1-DQA1 haplotype contain the etiological variants associated with AID. In GD this approach was successful in determining that DQB1 was unable to explain association with disease, narrowing down the location of the etiological variant within the class II region to either DRB1 or DQA1.

Sharing of susceptibility loci between AIDs is not unique to the HLA region with variants within CTLA-4, PTPN22 and CD25 also being shared. There are however distinct differences between the AIDs, with the DR15 (DRB1*15- DQB1*0602-DQA1*0102) haplotype strongly predisposing for MS, whilst protecting against T1D. The observation, therefore, of a number of different DR and/or DQ associations, with AID suggests that there are common and unique disease pathways for each AID which may, in part, be explained by the presentation of different disease-specific autoantigens.

HLA CLASS II DISEASE MECHANISMS

The role played by the HLA-DR/-DQ molecules in exogenous antigen presentation to CD4+ Th cells helps to explain their association with several AIDs (see Fig. 1). Exogenous peripheral antigens are internalized via antigen presenting cells (APC) and are degraded into 13-18 amino acid residue peptides, preferentially bound by HLA class II molecules, in the increasingly acidic compartments of the endocytic pathway. HLA class II molecules are synthesized in the rough endoplasmic reticulum (RER) where they associate with the invariant chain (Ii) to prevent endogenous peptide binding. The HLA class II molecule is then routed to the endocytic pathway, where Ii is degraded, leaving a short fragment of the Ii class II-associated invariant chain peptide (CLIP) bound, which is then exchanged for peptide. The HLA class II peptide complex is then transported to the cell surface for recognition by CD4+ Th cells, which determine whether an immune response is mounted. If an immune response is mounted CD4+ Th cells activate naive B cells to produce antibodies, or in the case of self-antigens autoantibodies, and aid in macrophage recruitment. Activated autoreactive CD4+ Th cells against a variety of exogenous autoantigens, including pancreatic beta cells, thyroid components and myelin, have been detected in TID, GD and MS respectively, suggesting a role in disease susceptibility.

Several non-mutually exclusive mechanisms have been proposed to explain association of DR/DQ with AIDs:

Variation in binding groves of associated DR/DQ molecules could lead to preferential presentation of only a specific limited set of self peptides or low affinity self peptides may allow autoreactive T cells to escape tolerance and enter the periphery. This could affect thymic T cell education, causing incomplete thymic tolerance and a Th and T regulatory (Treg) cell population that does not recognize all self molecules.

Polymorphic residues of the TCR-exposed surfaces of DR/DQ could select autoreactive T cells or fail to select a good Treg population. It has been proposed that the protective effects seen with specific HLA molecules could be due to the generation of Treg cells that are able to keep autoreactive T cells in check and prevent autoimmunity. Studies in RA have shown Treg populations to be compromised, suggesting that RA could be associated with a failure to protect rather than a predisposition to disease.

Promiscuous restriction where some TCRs will use a series of different restriction elements to bind to and, therefore, interact with a wider variety of different peptides.

Preferential binding in DR/DQ heterozygous subjects could be occurring through epitope stealing by one HLA molecule over another which, depending on TCR restriction of CD4+ Th cells, could affect whether an immune response is mounted.

Presentation of endogenous antigens by HLA class II. Although class II molecules traditionally present exogenous antigens and class I present endogenous antigens (see Fig. 1), this system is not absolute and presentation of endogenous antigens by class II and exogenous antigens by class I can be seen. This could alter how these antigens are presented to the immune system and the response triggered.

These hypotheses suggest a series of potential mechanistic pathways by which the HLA class II molecules could be involved in disease onset by altering the Th and Treg cell repertoire or through changes in how the antigen is recognized in the periphery.

EVIDENCE FOR ROLE OF HLA CLASS I IN DISEASE

Association of HLA class I molecules, in particular HLA-A, -B and –C, has been detected for several AIDs. HLA-B*27 has been known for many years to predispose to AS, and is present in over 90% of European AS patients. Of the 31 HLA-B*27 suballeles detected to date the B*2701, B*2704 and B*2705 alleles are strongly predisposing for AS, whereas the B*2706 and B*2709 alleles are protective. Interestingly, the B*2705 only differs from the B*2709 at amino acid residue 116, via an Asp or histidine (His), respectively, which is known to alter peptide specificity and T cell recognition. Although HLA-A, -B and –C are located in the HLA class I region, they exhibit LD with the HLA class II encoded DR/DQ haplotypes. The presence of this strong LD with the HLA class II region has made it difficult to identify independent effects for the class I region with any AIDs except AS which exhibits no strong class II associations, although further confirmation of potential HLA class II effects in AS is needed. The utilization of larger datasets and the development of more advanced statistical analysis, has enabled re-investigation of the HLA class I region as an independent general AID locus.

Work in T1D identified a microsatellite D6S2223 4.9kb telomeric of DQ in the extended class I region, as being associated with a reduction in the risk conferred by the DR3 extended haplotype on disease, with further work narrowing the association to a region encompassing the class III and HLA-B/-C gene regions. Work in the NOD mouse also suggested the presence of independent risk factors within the MHC, independent of the MHC class II, with further genetic studies in humans confirming the presence of HLA class II independent T1D susceptibility loci within the class I region. More recently, screening of a total of 1729 polymorphisms across the whole HLA region in several independent Caucasian T1D datasets, revealed evidence of a secondary peak of association for T1D independent of known DQB1 and DRB1 effects, due to the HLA-B locus (Pcombined = 2.01 x 10-19) with the B*39 allele consistently associated with T1D and some evidence for an effect of B*18. Association of HLA-A was also detected (Pcombined = 2.35 x 10-13), with predisposing effects for A*24 and protective effects for A*01, A*11 and A*31 identified.

The presence of additional susceptibility loci within the HLA class I gene region has also been detected for MS. HLA class II independent association of two microsatellite markers (D6S1683 and D6S265) in close proximity to the HLA class I region was reported. Association studies within a small Swedish dataset demonstrated a predisposing effect for the A*0301 allele and a protective effect for the A*0201 allele in patients with MS, independent of the known DR15 association, with further studies confirming the protective effect of A*0201. A recent large MS case control study further confirmed an independent protective effect of A*0201 (P = 7 x 10-12), although failed to detect an independent association for A*0301. Using a combination of microsatellite markers, tagging single nucleotide polymorphisms (SNPs) and classical HLA typing, the International MS genetics consortium detected an independent protective effect for C*05 (P = 3.3 x 10-5), in both a family and case control dataset. Although this study did not find any support for independent HLA-A effects, they could not rule out an effect at this locus. Interestingly when HLA-B and –C were screened for association with GD and logistic regression analysis applied to see if these effects were independent of known HLA-DR/-DQ affects, HLA-C, and to a lesser extent HLA-B, produced stronger association (P = 1.20 x 10-20 and P = 1.54 x 10-6, respectively) with disease than the previously established HLA class II effect, suggesting a key role in disease susceptibility.

HLA CLASS I DISEASE MECHANISMS

HLA class I molecules present endogenous antigens, such as those derived from viruses and intracellular bacteria, for recognition by the immune system (see Fig. 1). This process involves ubiquitination of endogenous cytosolic proteins and then degradation into short 8-16 amino acid peptides, optimal for HLA class I binding. These are subsequently transported into the RER where they bind HLA class I molecules combined with β2 microglobulin (β2M), before exiting the RER and being transported to the cell surface. HLA class I presented antigen is then recognized by CD8+ T cells and natural killer (NK) cells. Once CD8+ T cells become activated, functional effector T lymphocytes (CTLs) are produced which possess lytic capabilities and also play a role in generating CD8+ T memory cells, acting as part of both the innate and adaptive immune responses. Activated NKs act before clonal expansion and differentiation of CD8+ T cells and compliment the CTL response. They act as one of the first lines of innate immune defence by producing lymphokines, including interferons, which aid in the recruitment of additional cells to the site of inflammation and also produce cytokines and chemokines that have a cytolytic activity aiding cell destruction.

There is increasing evidence for a role of CD8+ T cells in AID. Knocking out MHC class I expression in the SLE prone mouse suggested an important role for CD8+ T cells in autoimmunity as it failed to develop SLE. Further models suggested a key role for CD8+ T cells in AID progression, rather than in initiation. Recently CD8+ T cells have been detected in the peripheral blood, cerebrospinal fluid and lesions of MS sufferers and were shown to destroy multiple central nervous system cell substrates, including myelin peptides. Suppressor CD8+ T cells have also been found to be decreased in relapsing MS subjects. Work in T1D has demonstrated CD8+ specific T cell responses and a potential role for defective CD8+ T suppressor cells with CD8+ T cells responses also shown to be important in SLE and GD.

Several hypotheses have been suggested to explain how variation in HLA class I genes could trigger autoimmunity. HLA class I molecules play a role in presenting endogenous antigens, including those derived from viruses and/or bacteria, which have been proposed to be key environmental triggers for AID (see Table 2 for a list of proposed viral triggers of AID). Viral/bacterial antigens may trigger AID through molecular mimicry and via acting as superantigens. Molecular mimicry occurs when microbial antigens that are sufficiently similar to self-antigens activate autoreactive T-cells that can cross react with self antigen triggering autoimmunity. Viral/bacterial antigens could also act as superantigens, producing a strong non-specific immune response that then cross reacts attacking other tissues in the body. Viruses can also alter HLA class I and II expression, potentially leading to greater antigen presentation to CD8+ T cells, with certain alleles more prone to viral/bacteria manipulation. During viral infection soluble HLA levels, involved in regulating the immune response, have also been shown to be increased in RA patients, the level of which is dependent on HLA allele present. If confirmed these mechanisms could also help validate the role of viral/bacterial infection in AID onset.

HLA class I molecules could also be associated with AID due to their role in inhibiting NK cell activity. NK cell cytotoxic activity is controlled by a balance between activating and inhibitory receptors on their surface. Activation signals are blocked by inhibitory signals produced through interaction of killer immunoglobulin-like receptors (KIR) with a variety of HLA class I molecules loaded with peptide. If HLA class I expression is normal then NK cell mediated destruction is inhibited. For example, there are two sets of KIRs, 2DL1 and 2DL2/2DL3 which recognize specific sets of HLA-C molecules, group C1 molecules (containing C*02, *04, *05 and *06) and group C2 molecules (containing C*01, *03, *07 and *08), respectively. Groups C1 and C2 are distinguished by the presence of Ser at position 77 and asparagine (Asn) at position 80 of the (1 helix or Asp at position 77 and a lysine (Lys) at position 80, respectively. KIR/HLA-C interactions can be altered by peptide loading and presentation by HLA-C, which could suggest that interaction seen in GD and MS of the associated HLA-C molecules with a given autoantigen/s could be affecting KIR binding and that this interaction between KIRs and HLA-C could play a role in autoimmune onset. Variation in the interaction of other molecules that bind to HLA class I and monitor HLA class I expression, including leukocyte Ig-like receptors (LIRs), members of the Ly49 family (Ly49) and the CD94/NKG2 family of receptors, could also provide another mechanism by which HLA class I could lead to AID.

Non-viral mechanisms have also been proposed including:

protein misfolding causing specific molecules to accumulate in the RER, where they are degraded, potentially causing a pro-inflammatory unfolded protein stress response or misfolded proteins themselves to become autoantigenic.

Conversion of HLA class I molecules into peptides which could then be presented by HLA class II molecules to the immune system and an immune response mounted as has been proposed in AS with B*27.

Peptide binding and presentation by specific HLA molecules as suggested earlier for HLA class II molecules with mechanisms including selection of antigen specific CD8+ T cells during thymic education, and positive or negative selection of a strong CD8+ T suppressor population.

ARE THERE ANY OTHER HLA ASSOCIATIONS?

Once the classical HLA class II and/or class I effects have been taken into account it becomes increasingly difficult to detect further associations, suggesting that even larger datasets and new techniques to cover more variation within this region are required. It should be noted that although HLA class II and class I appear to play a role in almost all AIDs, in some, the associations may lie outside of the classical loci. Strong association of HLA-C with psoriasis was detected and presumed to be the etiological variant, until further studies suggested that the true etiological variant actually lies 60kb outside of the HLA-C molecule. Although this review has focused on the classical HLA class I and II associations which have shown strong and consistent association with AID, several other genes within the HLA region may be acting as independent risk factors for AID (Table 3). Further work is required to determine if these genes are true AID etiological variants, using techniques, for example, which utilise the development of tag SNPs to screen the HLA region.

CONCLUSIONS

With our increased understanding of the complexity within the HLA region and the development of new statistical methodologies to help decipher the unique LD structure therein, progress has been made in starting to disentangle the associations present, providing valuable insights into AID mechanisms. Novel therapeutic treatments based on these discoveries have already been proposed. The development of protease inhibitors designed to alter the antigen presenting properties of HLA molecules, by blocking the presentation of potentially auto-antigenic peptides, could direct the immune system away from a particular antigenic motif and in turn the autoimmune disease process. Although clinical use may be some way off, continued research on the whole HLA region is vital to increase our understanding of the key mechanisms behind AID and ultimately the provision of new therapeutic targets.

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    Not in our library10.1007/bf02342437 (opens in a new tab)

  24. 24.

    Cucca F., Muntoni F., Lampis R., Frau F., Argiolas L., Silvetti M., Angius E., Cao A., De Virgiliis S., Congia M. Combinations of specific DRB1, DQA1, DQB1 haplotypes are associated with insulin-dependent diabetes mellitus in Sardinia. Hum. Immunol. 1993;37:85-94.

    Not in our library10.1016/0198-8859(93)90146-r (opens in a new tab)

  25. 25.

    Cucca F., Lampis R., Frau F., Macis D., Angius E., Masile P., Chessa M., Frongia P., Silvetti M., Cao A., De Virgiliis S., Congia M. The distribution of DR4 haplotypes in Sardinia suggests a primary association of type I diabetes with DRB1 and DQB1 loci. Hum. Immunol. 1995;43:301-308.

    Not in our library10.1016/0198-8859(95)00042-3 (opens in a new tab)

  26. 26.

    Cucca F., Lampis R., Congia M., Angius E., Nutland S., Bain S.C., Barnett A.H., Todd J.A. A correlation between the relative predisposition of MHC class II alleles to type 1 diabetes and the structure of their proteins. Hum. Mol. Genet. 2001;10:2025-2037.

    Not in our library10.1093/hmg/10.19.2025 (opens in a new tab)

  27. 27.

    Zhao Y., Dong Y., Zhu X., Qiu C. HLA-DRB1 alleles genotyping in patients with rheumatoid arthritis in Chinese. Chin. Med. Sci. J. 1996;11:232-235.

    Not in our library

  28. 28.

    Weyand C.M., McCarthy T.G., Goronzy J.J. Correlation between disease phenotype and genetic heterogeneity in rheumatoid arthritis. J. Clin. Invest. 1995;95:2120-2126.

    Not in our library10.1172/jci117900 (opens in a new tab)

  29. 29.

    Cavan D.A., Jacobs K.H., Penny M.A., Kelly M.A., Mijovic C., Jenkins D., Fletcher J.A., Barnett A.H. Both DQA1 and DQB1 genes are implicated in HLA-associated protection from type 1 (insulin-dependent) diabetes mellitus in a British Caucasian population. Diabetologia. 1993;36:252-257.

    Not in our library10.1007/bf00399959 (opens in a new tab)

  30. 30.

    Chelvanayagam G. A roadmap for HLA-DR peptide binding specificities. Hum. Immunol. 1997;58:61-69.

    Not in our library10.1016/s0198-8859(97)00185-7 (opens in a new tab)

  31. 31.

    Tait K.F., Gough S.C. The genetics of autoimmune endocrine disease. Clin. Endocrinol. (Oxf). 2003;59:1-11.

    Not in our library10.1046/j.1365-2265.2003.01723.x (opens in a new tab)

  32. 32.

    Simmonds M.J., Howson J.M., Heward J.M., Carr-Smith J., Franklyn J.A., Todd J.A., Gough S.C. A novel and major association of HLA-C in Graves' disease that eclipses the classical HLA-DRB1 effect. Hum. Mol. Genet. 2007;16:2149-2153.

    Not in our library10.1093/hmg/ddm165 (opens in a new tab)

  33. 33.

    Brand O.J., Lowe C.E., Heward J.M., Franklyn J.A., Cooper J.D., Todd J.A., Gough S.C.L. Association of the interleukin-2 receptor alpha (IL-2R?)/CD25 gene region with Graves' disease using a multilocus test and tag SNPs. Clin. Endocrinol. (Oxf). 2007;66:508-512.

    Not in our library10.1111/j.1365-2265.2007.02762.x (opens in a new tab)

  34. 34.

    Lowe C.E., Cooper J.D., Brusko T., Walker N.M., Smyth D.J., Bailey R., Bourget K., Plagnol V., Field S., Atkinson M., Clayton D.G., Wicker L.S., Todd J.A. Large-scale genetic fine mapping and genotype-phenotype associations implicate polymorphism in the IL2RA region in type 1 diabetes. Nat. Genet. 2007;39:1074-1082.

    Not in our library10.1038/ng2102 (opens in a new tab)

  35. 35.

    Vella A., Cooper J.D., Lowe C.E., Walker N., Nutland S., Widmer B., Jones R., Ring S.M., McArdle W., Pembrey M.E., Strachan D.P., Dunger D.B., Twells R.C., Clayton D.G., Todd J.A. Localization of a type 1 diabetes locus in the IL2RA/CD25 region by use of tag single-nucleotide polymorphisms. Am. J. Hum. Genet. 2005;76:773-779.

    Not in our library10.1086/429843 (opens in a new tab)

  36. 36.

    Giordano M., D'Alfonso S., Momigliano-Richiardi P. Genetics of multiple sclerosis: linkage and association studies. Am. J. Pharmacogenomics. 2002;2:37-58.

    Not in our library10.2165/00129785-200202010-00004 (opens in a new tab)

  37. 37.

    Villadangos J.A. Presentation of antigens by MHC class II molecules: getting the most out of them. Mol. Immunol. 2001;38:329-346.

    Not in our library10.1016/s0161-5890(01)00069-4 (opens in a new tab)

  38. 38.

    Nielsen C.H., Moeller A.C., Hegedus L., Bendtzen K., Leslie R.G. Self-reactive CD4+ T cells and B cells in the blood in health and autoimmune disease: increased frequency of thyroglobulin-reactive cells in Graves' disease. J Clin Immunol. 2006;26:126-137.

    Not in our library10.1007/s10875-006-9000-z (opens in a new tab)

  39. 39.

    Zanelli E., Breedveld F.C., de Vries R.R. HLA association with autoimmune disease: a failure to protect? Rheumatology (Oxford). 2000;39:1060-1066.

    Not in our library10.1093/rheumatology/39.10.1060 (opens in a new tab)

  40. 40.

    Ehrenstein M.R., Evans J.G., Singh A., Moore S., Warnes G., Isenberg D.A., Mauri C. Compromised function of regulatory T cells in rheumatoid arthritis and reversal by anti-TNFalpha therapy. J. Exp. Med. 2004;200:277-285.

    Not in our library10.1084/jem.20040165 (opens in a new tab)

  41. 41.

    Ettinger R.A., Papadopoulos G.K., Moustakas A.K., Nepom G.T., Kwok W.W. Allelic Variation in Key Peptide-Binding Pockets Discriminates between Closely Related Diabetes-Protective and Diabetes-Susceptible HLA-DQB1*06 Alleles. J. Immunol. 2006;176:1988-1998.

    Not in our library10.4049/jimmunol.176.3.1988 (opens in a new tab)

  42. 42.

    Gromme M., Neefjes J. Antigen degradation or presentation by MHC class I molecules via classical and non-classical pathways. Mol. Immunol. 2002;39:181-202.

    Not in our library10.1016/s0161-5890(02)00101-3 (opens in a new tab)

  43. 43.

    Parham P. Presentation of HLA class I-derived peptides: potential involvement in allorecognition and HLA-B27-associated arthritis. Immunol. Rev. 1996;154:137-154.

    Not in our library10.1111/j.1600-065x.1996.tb00932.x (opens in a new tab)

  44. 44.

    Reveille J.D., Ball E.J., Khan M.A. HLA-B27 and genetic predisposing factors in spondyloarthropathies. Curr. Opin. Rheumatol. 2001;13:265-272.

    Not in our library10.1097/00002281-200107000-00004 (opens in a new tab)

  45. 45.

    Khan M.A., Mathieu A., Sorrentino R., Akkoc N. The pathogenetic role of HLA-B27 and its subtypes. Autoimmun. Rev. 2007;6:183-189.

    Not in our library10.1016/j.autrev.2006.11.003 (opens in a new tab)

  46. 46.

    Khan M.A. Update on spondyloarthropathies. Ann. Intern. Med. 2002;136:896-907.

    Not in our library10.7326/0003-4819-136-12-200206180-00011 (opens in a new tab)

  47. 47.

    Paladini F., Taccari E., Fiorillo M.T., Cauli A., Passiu G., Mathieu A., Punzi L., Lapadula G., Scarpa R., Sorrentino R. Distribution of HLA-B27 subtypes in Sardinia and continental Italy and their association with spondylarthropathies. Arthritis Rheum. 2005;52:3319-3321.

    Not in our library10.1002/art.21308 (opens in a new tab)

  48. 48.

    Reveille J.D. Major histocompatibility genes and ankylosing spondylitis. Best Pract. Res. Clin. Rheumatol. 2006;20:601-609.

    Not in our library10.1016/j.berh.2006.03.004 (opens in a new tab)

  49. 49.

    Brown M.A., Kennedy L.G., Darke C., Gibson K., Pile K.D., Shatford J.L., Taylor A., Calin A., Wordsworth B.P. The effect of HLA-DR genes on susceptibility to and severity of ankylosing spondylitis. Arthritis Rheum. 1998;41:460-465.

    Not in our library10.1002/1529-0131(199803)41:3<460::aid-art12>3.0.co;2-x (opens in a new tab)

  50. 50.

    Lie B.A., Todd J.A., Pociot F., Nerup J., Akselsen H.E., Joner G., Dahl-Jorgensen K., Ronningen K.S., Thorsby E., Undlien D.E. The predisposition to type 1 diabetes linked to the human leukocyte antigen complex includes at least one non-class II gene. Am. J. Hum. Genet. 1999;64:793-800.

    Not in our library10.1086/302283 (opens in a new tab)

  51. 51.

    Johansson S., Lie B.A., Todd J.A., Pociot F., Nerup J., Cambon-Thomsen A., Kockum I., Akselsen H.E., Thorsby E., Undlien D.E. Evidence of at least two type 1 diabetes susceptibility genes in the HLA complex distinct from HLA-DQB1, -DQA1 and -DRB1. Genes Immun. 2003;4:46-53.

    Not in our library10.1038/sj.gene.6363917 (opens in a new tab)

  52. 52.

    Boulard O., Damotte D., Deruytter N., Fluteau G., Carnaud C., Garchon H.J. An interval tightly linked to but distinct from the H2 complex controls both overt diabetes (Idd16) and chronic experimental autoimmune thyroiditis (Ceat1) in nonobese diabetic mice. Diabetes. 2002;51:2141-2147.

    Not in our library10.2337/diabetes.51.7.2141 (opens in a new tab)

  53. 53.

    Valdes A.M., Erlich H.A., Noble J.A. Human leukocyte antigen class I B and C loci contribute to Type 1 Diabetes (T1D) susceptibility and age at T1D onset. Hum. Immunol. 2005;66:301-313.

    Not in our library10.1016/j.humimm.2004.12.001 (opens in a new tab)

  54. 54.

    Windsor L., Puschendorf M., Allcock R., Scott A., Sayer D., Kucharzak R., Gut I., McCann V., Davis E., Witt C., Christiansen F., Price P. Does a central MHC gene in linkage disequilibrium with HLA-DRB1*0401 affect susceptibility to type 1 diabetes? Genes Immun. 2005;6:298-304.

    Not in our library10.1038/sj.gene.6364210 (opens in a new tab)

  55. 55.

    Nejentsev S., Howson J.M., Walker N.M., Szeszko J., Field S.F., Stevens H.E., Reynolds P., Hardy M., King E., Masters J., Hulme J., Maier L.M., Smyth D., Bailey R., Cooper J.D., Ribas G., Campbell R.D., Clayton D.G., Todd J.A., Burton P.R., Clayton D.G., Cardon L.R., Craddock N., Deloukas P., Duncanson A., Kwiatkowski D.P., McCarthy M.I., Ouwehand W.H., Samani N.J., Todd J.A., Donnelly Chair P., Barrett J.C., Burton P.R., Davison D., Donnelly P., Easton D., Evans D., Leung H.T., Marchini J.L., Morris A.P., Spencer C.C., Tobin M.D., Cardon Co-Chair L.R., Clayton Co-Chair D.G., Attwood A.P., Boorman J.P., Cant B., Everson U., Hussey J.M., Jolley J.D., Knight A.S., Koch K., Meech E., Nutland S., Prowse C.V., Stevens H.E., Taylor N.C., Walters G.R., Walker N.M., Watkins N.A., Winzer T., Todd J.A., Ouwehand W.H., Jones R.W., McArdle W.L., Ring S.M., Strachan D.P., Pembrey M., Breen G., St Clair Aberdeen D., Caesar S., Gordon-Smith K., Jones Birmingham L., Fraser C., Green E.K., Grozeva D., Hamshere M.L., Holmans P.A., Jones I.R., Kirov G., Moskvina V., Nikolov I., O'Donovan M.C., Owen M.J., Craddock Cardiff N., Collier D.A., Elkin A., Farmer A., Williamson R., McGuffin London P., Young A.H., Nicol Ferrier Newcastle I., Ball S.G., Balmforth A.J., Barrett J.H., Bishop D.T., Iles M.M., Maqbool A., Yuldasheva N., Hall Leeds A.S., Braund P.S., Burton P.R., Dixon R.J., Mangino M., Stevens S., Tobin M.D., Thompson J.R., Samani Leicester N.J., Bredin F., Tremelling M., Parkes Cambridge M., Drummond H., Lees C.W., Nimmo E.R., Satsangi Edinburgh J., Fisher S.A., Forbes A., Lewis C.M., Onnie C.M., Prescott N.J., Sanderson J., Mathew London C.G., Barbour J., Khalid Mohiuddin M., Todhunter C.E., Mansfield Newcastle J.C., Ahmad T., Cummings F.R., Jewell Oxford D.P., Webster Aberdeen J., Brown M.J., Clayton Cambridge D.G., Lathrop Evry France G.M., Connell J., Dominiczak Glasgow A., Samani Leicester N.J., Braga Marcano C.A., Burke B., Dobson R., Gungadoo J., Lee K.L., Munroe P.B., Newhouse S.J., Onipinla A., Wallace C., Xue M., Caulfield London M., Farrall Oxford M., Barton A., Bruce I.N., Donovan H., Eyre S., Gilbert P.D., Hider S.L., Hinks A.M., John S.L., Potter C., Silman A.J., Symmons D.P., Thomson W., Worthington J., Clayton D.G., Dunger D.B., Nutland S., Stevens H.E., Walker N.M., Widmer B., Todd J.A., Frayling T.M., Freathy R.M., Lango H., Perry J.R., Shields B.M., Weedon M.N., Hattersley Exeter A.T., Hitman London G.A., Walker Newcastle M., Elliott K.S., Groves C.J., Lindgren C.M., Rayner N.W., Timpson N.J., Zeggini E., McCarthy Oxford M.I., Newport M., Sirugo Gambia G., Lyons E., Vannberg F., Hill Oxford A.V., Bradbury L.A., Farrar C., Pointon J.J., Wordsworth P., Brown M.A., Franklyn J.A., Heward J.M., Simmonds M.J., Gough S.C., Seal S., Stratton M.R., Rahman N., Ban M., Goris A., Sawcer S.J., Compston A., Conway D., Jallow M., Newport M., Sirugo Gambia G., Rockett K.A., Kwiatkowski Oxford D.P., Bryan C., Bumpstead S.J., Chaney A., Downes K., Ghori J., Gwilliam R., Hunt S.E., Inouye M., Keniry A., King E., McGinnis R., Potter S., Ravindrarajah R., Whittaker P., Withers D., Deloukas P., Leung H.T., Nutland S., Stevens H.E., Walker N.M., Todd Cambridge J.A., Easton D., Clayton Cambridge D.G., Burton P.R., Tobin Leicester M.D., Barrett J.C., Evans D., Morris A.P., Cardon L.R., Cardin N.J., Davison D., Ferreira T., Pereira-Gale J., Hallgrimsdottir I.B., Howie B.N., Marchini J.L., Spencer C.C., Su Z., Ying Teo Y., Vukcevic D., Donnelly Oxford P., Bentley D., Brown M.A., Cardon L.R., Caulfield M., Clayton D.G., Compston A., Craddock N., Deloukas P., Donnelly P., Farrall M., Gough S.C., Hall A.S., Hattersley A.T., Hill A.V., Kwiatkowski D.P., Mathew C.G., McCarthy M.I., Ouwehand W.H., Parkes M., Pembrey M., Rahman N., Samani N.J., Stratton M.R., Todd J.A., Worthington J. Localization of type 1 diabetes susceptibility to the MHC class I genes HLA-B and HLA-A. Nature. 2007.

    Not in our library10.1038/nature06406 (opens in a new tab)

  56. 56.

    Marrosu M.G., Murru R., Murru M.R., Costa G., Zavattari P., Whalen M., Cocco E., Mancosu C., Schirru L., Solla E., Fadda E., Melis C., Porru I., Rolesu M., Cucca F. Dissection of the HLA association with multiple sclerosis in the founder isolated population of Sardinia. Hum. Mol. Genet. 2001;10:2907-2916.

    Not in our library10.1093/hmg/10.25.2907 (opens in a new tab)

  57. 57.

    Fogdell-Hahn A., Ligers A., Gronning M., Hillert J., Olerup O. Multiple sclerosis a modifying influence of HLA class I genes in an HLA class II associated autoimmune disease. Tissue Antigens. 2000;55:140-148.

    Not in our library10.1034/j.1399-0039.2000.550205.x (opens in a new tab)

  58. 58.

    Harbo H.F., Lie B.A., Sawcer S., Celius E.G., Dai K.Z., Oturai A., Hillert J., Lorentzen A.R., Laaksonen M., Myhr K.M., Ryder L.P., Fredrikson S., Nyland H., Sorensen P.S., Sandberg-Wollheim M., Andersen O., Svejgaard A., Edland A., Mellgren S.I., Compston A., Vartdal F., Spurkland A. Genes in the HLA class I region may contribute to the HLA class II-associated genetic susceptibility to multiple sclerosis. Tissue Antigens. 2004;63:237-247.

    Not in our library10.1111/j.0001-2815.2004.00173.x (opens in a new tab)

  59. 59.
    HLA-A Confers an HLA-DRB1 Independent Influence on the Risk of Multiple Sclerosis · 2007
    No notice
  60. 60.
    A second major histocompatibility complex susceptibility locus for multiple sclerosis · 2007
    No notice
  61. 61.

    Sawicki M.W., Dimasi N., Natarajan K., Wang J., Margulies D.H., Mariuzza R.A. Structural basis of MHC class I recognition by natural killer cell receptors. Immunol. Rev. 2001;181:52-65.

    Not in our library10.1034/j.1600-065x.2001.1810104.x (opens in a new tab)

  62. 62.

    Mozes E., Kohn L.D., Hakim F., Singer D.S. Resistance of MHC class I-deficient mice to experimental systemic lupus erythematosus. Science. 1993;261:91-93.

    Not in our library10.1126/science.8316860 (opens in a new tab)

  63. 63.

    Singer D.S., Mozes E., Kirshner S., Kohn L.D. Role of MHC class I molecules in autoimmune disease. Crit. Rev. Immunol. 1997;17:463-468.

    Not in our library

  64. 64.

    Singer D.S., Zinger H., Kohn L.D., Mozes E. Differing MHC class I requirements for induction and propagation of experimental systemic lupus erythematosus. Eur. J. Immunol. 1999;29:2259-2268.

    Not in our library10.1002/(sici)1521-4141(199907)29:07<2259::aid-immu2259>3.0.co;2-1 (opens in a new tab)

  65. 65.

    Johnson A.J., Suidan G.L., McDole J., Pirko I. The CD8 T cell in multiple sclerosis: suppressor cell or mediator of neuropathology? Int. Rev. Neurobiol. 2007;79:73-97.

    Not in our library10.1016/s0074-7742(07)79004-9 (opens in a new tab)

  66. 66.

    McDole J., Johnson A.J., Pirko I. The role of CD8+ T-cells in lesion formation and axonal dysfunction in multiple sclerosis. Neurol. Res. 2006;28:256-261.

    Not in our library10.1179/016164106x98125 (opens in a new tab)

  67. 67.

    Togun R.A., Resetkova E., Kawai K., Enomoto T., Volpe R. Activation of CD8+ T lymphocytes in insulin-dependent diabetes mellitus. Clin. Immunol. Immunopathol. 1997;82:243-249.

    Not in our library10.1006/clin.1996.4295 (opens in a new tab)

  68. 68.

    Toma A., Haddouk S., Briand J.P., Camoin L., Gahery H., Connan F., Dubois-Laforgue D., Caillat-Zucman S., Guillet J.G., Carel J.C., Muller S., Choppin J., Boitard C. Recognition of a subregion of human proinsulin by class I-restricted T cells in type 1 diabetic patients. Proc. Natl. Acad. Sci. USA. 2005;102:10581-10586.

    Not in our library10.1073/pnas.0504230102 (opens in a new tab)

  69. 69.

    Hassainya Y., Garcia-Pons F., Kratzer R., Lindo V., Greer F., Lemonnier F.A., Niedermann G., van Endert P.M. Identification of naturally processed HLA-A2--restricted proinsulin epitopes by reverse immunology. Diabetes. 2005;54:2053-2059.

    Not in our library10.2337/diabetes.54.7.2053 (opens in a new tab)

  70. 70.

    Walter U., Santamaria P. CD8+ T cells in autoimmunity. Curr. Opin. Immunol. 2005;17:624-631.

    Not in our library10.1016/j.coi.2005.09.014 (opens in a new tab)

  71. 71.

    Moller E. Mechanisms for induction of autoimmunity in humans. Acta. Paediatr. Suppl. 1998;424:16-20.

    Not in our library10.1111/j.1651-2227.1998.tb01228.x (opens in a new tab)

  72. 72.

    Bowness P. HLA B27 in health and disease a double-edged sword? Rheumatology (Oxford). 2002;41:857-868.

    Not in our library10.1093/rheumatology/41.8.857 (opens in a new tab)

  73. 73.

    Suzuki K., Mori A., Ishii K.J., Saito J., Singer D.S., Klinman D.M., Krause P.R., Kohn L.D. Activation of target-tissue immune-recognition molecules by double-stranded polynucleotides. Proc. Natl. Acad. Sci. USA. 1999;96:2285-2290.

    Not in our library10.1073/pnas.96.5.2285 (opens in a new tab)

  74. 74.

    McDonald J.C., Adamashvili I. Soluble HLA a review of the literature. Hum. Immunol. 1998;59:387-403.

    Not in our library10.1016/s0198-8859(98)00033-0 (opens in a new tab)

  75. 75.

    Tabayoyong W.B., Zavazava N. Soluble HLA revisited. Leuk. Res. 2007;31:121-125.

    Not in our library10.1016/j.leukres.2006.06.008 (opens in a new tab)

  76. 76.

    Radaev S., Sun P.D. Structure and function of natural killer cell surface receptors. Annu. Rev. Biophys. Biomol. Struct. 2003;32:93-114.

    Not in our library10.1146/annurev.biophys.32.110601.142347 (opens in a new tab)

  77. 77.

    Deng L., Mariuzza R.A. Structural basis for recognition of MHC and MHC-like ligands by natural killer cell receptors. Semin. Immunol. 2006;18:159-166.

    Not in our library10.1016/j.smim.2006.03.004 (opens in a new tab)

  78. 78.

    Bashirova A.A., Martin M.P., McVicar D.W., Carrington M. The Killer Immunoglobulin-Like Receptor Gene Cluster Tuning the Genome for Defense (*). Annu. Rev. Genomics Hum. Genet. 2006;7:277-300.

    Not in our library10.1146/annurev.genom.7.080505.115726 (opens in a new tab)

  79. 79.

    Malnati M.S., Peruzzi M., Parker K.C., Biddison W.E., Ciccone E., Moretta A., Long E.O. Peptide specificity in the recognition of MHC class I by natural killer cell clones. Science. 1995;267:1016-1018.

    Not in our library10.1126/science.7863326 (opens in a new tab)

  80. 80.
    Self and viral peptides can initiate lysis by autologous natural killer cells · 1997
    Not checked
  81. 81.

    van der Slik A.R., Koeleman B.P., Verduijn W., Bruining G.J., Roep B.O., Giphart M.J. KIR in type 1 diabetes disparate distribution of activating and inhibitory natural killer cell receptors in patients versus HLA-matched control subjects. Diabetes. 2003;52:2639-2642.

    Not in our library10.2337/diabetes.52.10.2639 (opens in a new tab)

  82. 82.

    Martin M.P., Nelson G., Lee J.H., Pellett F., Gao X., Wade J., Wilson M.J., Trowsdale J., Gladman D., Carrington M. Cutting edge susceptibility to psoriatic arthritis influence of activating killer Ig-like receptor genes in the absence of specific HLA-C alleles. J. Immunol. 2002;169:2818-2822.

    Not in our library10.4049/jimmunol.169.6.2818 (opens in a new tab)

  83. 83.

    Borges L., Hsu M.L., Fanger N., Kubin M., Cosman D. A family of human lymphoid and myeloid Ig-like receptors, some of which bind to MHC class I molecules. J. Immunol. 1997;159:5192-5196.

    Not in our library

  84. 84.

    Vukmanovic S., Neubert T.A., Santori F.R. Could TCR antagonism explain associations between MHC genes and disease? Trends Mol. Med. 2003;9:139-146.

    Not in our library10.1016/s1471-4914(03)00029-7 (opens in a new tab)

  85. 85.

    Nair R.P., Stuart P., Henseler T., Jenisch S., Chia N.V., Westphal E., Schork N.J., Kim J., Lim H.W., Christophers E., Voorhees J.J., Elder J.T. Localization of psoriasis-susceptibility locus PSORS1 to a 60-kb interval telomeric to HLA-C. Am. J. Hum. Genet. 2000;66:1833-1844.

    Not in our library10.1086/302932 (opens in a new tab)

  86. 86.

    Lie B.A., Thorsby E. Several genes in the extended human MHC contribute to predisposition to autoimmune diseases. Curr. Opin. Immunol. 2005;17:526-531.

    Not in our library10.1016/j.coi.2005.07.001 (opens in a new tab)

  87. 87.

    Burton P.R., Clayton D.G., Cardon L.R., Craddock N., Deloukas P., Duncanson A., Kwiatkowski D.P., McCarthy M.I., Ouwehand W.H., Samani N.J., Todd J.A., Donnelly Chair P., Barrett J.C., Burton P.R., Davison D., Donnelly P., Easton D., Evans D.M., Leung H.T., Marchini J.L., Morris A.P., Spencer C.C., Tobin M.D., Cardon L.R., Clayton D.G., Attwood A.P., Boorman J.P., Cant B., Everson U., Hussey J.M., Jolley J.D., Knight A.S., Koch K., Meech E., Nutland S., Prowse C.V., Stevens H.E., Taylor N.C., Walters G.R., Walker N.M., Watkins N.A., Winzer T., Todd J.A., Ouwehand W.H., Jones R.W., McArdle W.L., Ring S.M., Strachan D.P., Pembrey M., Breen G., Clair D.S., Caesar S., Gordon-Smith K., Jones L., Fraser C., Green E.K., Grozeva D., Hamshere M.L., Holmans P.A., Jones I.R., Kirov G., Moskivina V., Nikolov I., O'Donovan M.C., Owen M.J., Craddock N., Collier D.A., Elkin A., Farmer A., Williamson R., McGuffin P., Young A.H., Ferrier I.N., Ball S.G., Balmforth A.J., Barrett J.H., Bishop T.D., Iles M.M., Maqbool A., Yuldasheva N., Hall A.S., Braund P.S., Burton P.R., Dixon R.J., Mangino M., Stevens S., Tobin M.D., Thompson J.R., Samani N.J., Bredin F., Tremelling M., Parkes M., Drummond H., Lees C.W., Nimmo E.R., Satsangi J., Fisher S.A., Forbes A., Lewis C.M., Onnie C.M., Prescott N.J., Sanderson J., Matthew C.G., Barbour J., Mohiuddin M.K., Todhunter C.E., Mansfield J.C., Ahmad T., Cummings F.R., Jewell D.P., Webster J., Brown M.J., Clayton D.G., Lathrop M.G., Connell J., Dominiczak A., Samani N.J., Marcano C.A., Burke B., Dobson R., Gungadoo J., Lee K.L., Munroe P.B., Newhouse S.J., Onipinla A., Wallace C., Xue M., Caulfield M., Farrall M., Barton A., Bruce I.N., Donovan H., Eyre S., Gilbert P.D., Hilder S.L., Hinks A.M., John S.L., Potter C., Silman A.J., Symmons D.P., Thomson W., Worthington J., Clayton D.G., Dunger D.B., Nutland S., Stevens H.E., Walker N.M., Widmer B., Todd J.A., Frayling T.M., Freathy R.M., Lango H., Perry J.R., Shields B.M., Weedon M.N., Hattersley A.T., Hitman G.A., Walker M., Elliott K.S., Groves C.J., Lindgren C.M., Rayner N.W., Timpson N.J., Zeggini E., McCarthy M.I., Newport M., Sirugo G., Lyons E., Vannberg F., Hill A.V., Bradbury L.A., Farrar C., Pointon J.J., Wordsworth P., Brown M.A., Franklyn J.A., Heward J.M., Simmonds M.J., Gough S.C., Seal S., Stratton M.R., Rahman N., Ban M., Goris A., Sawcer S.J., Compston A., Conway D., Jallow M., Newport M., Sirugo G., Rockett K.A., Kwiatkowski D.P., Bumpstead S.J., Chaney A., Downes K., Ghori M.J., Gwilliam R., Hunt S.E., Inouye M., Keniry A., King E., McGinnis R., Potter S., Ravindrarajah R., Whittaker P., Widden C., Withers D., Deloukas P., Leung H.T., Nutland S., Stevens H.E., Walker N.M., Todd J.A., Easton D., Clayton D.G., Burton P.R., Tobin M.D., Barrett J.C., Evans D.M., Morris A.P., Cardon L.R., Cardin N.J., Davison D., Ferreira T., Pereira-Gale J., Hallgrimsdottir I.B., Howie B.N., Marchini J.L., Spencer C.C., Su Z., Teo Y.Y., Vukcevic D., Donnelly P., Bentley D., Brown M.A., Cardon L.R., Caulfield M., Clayton D.G., Compston A., Craddock N., Deloukas P., Donnelly P., Farrall M., Gough S.C., Hall A.S., Hattersley A.T., Hill A.V., Kwiatkowski D.P., Matthew C.G., McCarthy M.I., Ouwehand W.H., Parkes M., Pembrey M., Rahman N., Samani N.J., Stratton M.R., Todd J.A., Worthington J., Mitchell S.L., Newby P.R., Brand O.J., Carr-Smith J., Pearce S.H., Gough S.C., McGinnis R., Keniry A., Deloukas P., Reveille J.D., Zhou X., Bradbury L.A., Sims A.M., Dowling A., Taylor J., Doan T., Cardon L.R., Davis J.C., Pointon J.J., Savage L., Ward M.M., Learch T.L., Weisman M.H., Wordsworth P., Brown M.A. Association scan of 14,500 nonsynonymous SNPs in four diseases identifies autoimmunity variants. Nat. Genet. 2007;39:1329-1337.

    Not in our library10.1038/ng.2007.17 (opens in a new tab)

  88. 88.

    Wellcome Trust Case Control Consortium.Genome-wide association study f 1400 cases of seven common diseases and 3,000 shared controls. Nature. 2007;447:661-678.

    Not in our library10.1038/nature05911 (opens in a new tab)

  89. 89.

    de Bakker P.I., McVean G., Sabeti P.C., Miretti M.M., Green T., Marchini J., Ke X., Monsuur A.J., Whittaker P., Delgado M., Morrison J., Richardson A., Walsh E.C., Gao X., Galver L., Hart J., Hafler D.A., Pericak-Vance M., Todd J.A., Daly M.J., Trowsdale J., Wijmenga C., Vyse T.J., Beck S., Murray S.S., Carrington M., Gregory S., Deloukas P., Rioux J.D. A high-resolution HLA and SNP haplotype map for disease association studies in the extended human MHC. Nat. Genet. 2006;38:1166-1172.

    Not in our library10.1038/ng1885 (opens in a new tab)

  90. 90.

    Miretti M.M., Walsh E.C., Ke X., Delgado M., Griffiths M., Hunt S., Morrison J., Whittaker P., Lander E.S., Cardon L.R., Bentley D.R., Rioux J.D., Beck S., Deloukas P. A high-resolution linkage-disequilibrium map of the human major histocompatibility complex and first generation of tag single-nucleotide polymorphisms. Am. J. Hum. Genet. 2005;76:634-646.

    Not in our library10.1086/429393 (opens in a new tab)

  91. 91.

    Pichurin P., Pham N., David C.S., Rapoport B., McLachlan S.M. HLA-DR3 transgenic mice immunized with adenovirus encoding the thyrotropin receptor T cell epitopes and functional analysis of the CD40 Graves' polymorphism. Thyroid. 2006;16:1221-1227.

    Not in our library10.1089/thy.2006.16.1221 (opens in a new tab)

  92. 92.

    Dotta F., Censini S., van Halteren A.G., Marselli L., Masini M., Dionisi S., Mosca F., Boggi U., Muda A.O., Prato S.D., Elliott J.F., Covacci A., Rappuoli R., Roep B.O., Marchetti P. Coxsackie B4 virus infection of beta cells and natural killer cell insulitis in recent-onset type 1 diabetic patients. Proc. Natl. Acad. Sci. USA. 2007;104:5115-5120.

    Not in our library10.1073/pnas.0700442104 (opens in a new tab)

  93. 93.

    Maha M.M., Ali M.A., Abdel-Rehim S.E., Abu-Shady E.A., El-Naggar B.M., Maha Y.Z. The role of coxsackieviruses infection in the children of insulin dependent diabetes mellitus. J. Egypt Public Health Assoc. 2003;78:305-318.

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  94. 94.

    Green J., Casabonne D., Newton R. Coxsackie B virus serology and Type 1 diabetes mellitus a systematic review of published case-control studies. Diabet. Med. 2004;21:507-514.

    Not in our library10.1111/j.1464-5491.2004.01182.x (opens in a new tab)

  95. 95.

    Banatvala J.E. Insulin-dependent (juvenile-onset, type 1) diabetes mellitus Coxsackie B viruses revisited. Prog. Med. Virol. 1987;34:33-54.

    Not in our library

  96. 96.

    Zandman-Goddard G., Shoenfeld Y. Infections and SLE. Autoimmunity. 2005;38:473-485.

    Not in our library10.1080/08916930500285352 (opens in a new tab)

  97. 97.

    Guiserix J. Systemic lupus erythematosus following hepatitis B vaccine. Nephron. 1996;74:441.

    Not in our library10.1159/000189357 (opens in a new tab)

  98. 98.

    Eddy S., Wim R., Peter V.E., Tanja R., Jan T., Werner V.S. Myasthenia gravis another autoimmune disease associated with hepatitis C virus infection. Dig. Dis. Sci. 1999;44:186-189.

    Not in our library10.1023/a:1026683007277 (opens in a new tab)

  99. 99.

    Halfon P., Levy M., San Marco M., Gerolami V., Khiri H., Bourliere M., Feryn J.M., Gastaut J.L., Pouget J., Cartouzou G. Myasthenia gravis and hepatitis C virus infection. J. Viral Hepat. 1996;3:329-332.

    Not in our library10.1111/j.1365-2893.1996.tb00106.x (opens in a new tab)

  100. 100.

    Jadali Z., Esfahanian F., Eslami M.B., Sanati M.H. Serum Antibodies against Hepatitis C Virus in Iranian Patients with Graves' Disease. Iran J. Allergy Asthma Immunol. 2005;4:91-94.

    Not in our library

  101. 101.

    Leri O., Sinopoli M.T., Di Prima M.A., Paggi A. Hepatitis C virus antibodies and Graves' disease. Bmj. 1995;310:128-129.

    Not in our library10.1136/bmj.310.6972.128d (opens in a new tab)

  102. 102.

    Masuda H., Atsumi T., Fujisaku A., Shimizu C., Yoshioka N., Koike T. Acute onset of type 1 diabetes accompanied by acute hepatitis C the potential role of proinflammatory cytokine in the pathogenesis of autoimmune diabetes. Diabetes Res. Clin. Pract. 2007;75:357-361.

    Not in our library10.1016/j.diabres.2006.07.016 (opens in a new tab)

  103. 103.

    Chen L.K., Chou Y.C., Tsai S.T., Hwang S.J., Lee S.D. Hepatitis C virus infection-related Type 1 diabetes mellitus. Diabet. Med. 2005;22:340-343.

    Not in our library10.1111/j.1464-5491.2005.01412.x (opens in a new tab)

  104. 104.

    Ahmed M.M., Berney S.M., Wolf R.E., Hearth-Holmes M., Hayat S., Mubashir E., Vanderheyde H., Chang W.L., King J.W. Prevalence of active hepatitis C virus infection in patients with systemic lupus erythematosus. Am. J. Med. Sci. 2006;331:252-256.

    Not in our library10.1097/00000441-200605000-00003 (opens in a new tab)

  105. 105.

    Christensen T. Human herpesviruses in MS. Int. MS J. 2007;14:41-47.

    Not in our library

  106. 106.

    Hawkes C.H., Giovannoni G., Keir G., Cunnington M., Thompson E.J. Seroprevalence of herpes simplex virus type 2 in multiple sclerosis. Acta. Neurol. Scand. 2006;114:363-367.

    Not in our library10.1111/j.1600-0404.2006.00677.x (opens in a new tab)

  107. 107.

    Ross R.T. The varicella-zoster virus and multiple sclerosis. J. Clin. Epidemiol. 1998;51:533-535.

    Not in our library10.1016/s0895-4356(98)00030-4 (opens in a new tab)

  108. 108.

    Barzilai O., Sherer Y., Ram M., Izhaky D., Anaya J.M., Shoenfeld Y. Epstein-Barr virus and cytomegalovirus in autoimmune diseases are they truly notorious?.A preliminary report. Ann. N Y Acad. Sci. 2007;1108:567-577.

    Not in our library10.1196/annals.1422.059 (opens in a new tab)

  109. 109.

    Toussirot E., Roudier J. Pathophysiological links between rheumatoid arthritis and the Epstein-Barr virus: an update. Joint Bone Spine. 2007;74:418-426.

    Not in our library10.1016/j.jbspin.2007.05.001 (opens in a new tab)

  110. 110.

    Sawada S., Takei M. Possible involvement of Epstein-Barr virus and its regulatory gene in rheumatoid synovitis. Autoimmun. Rev. 2004;3(Suppl 1):S69-71.

    Not in our library

  111. 111.

    Banwell B., Krupp L., Kennedy J., Tellier R., Tenembaum S., Ness J., Belman A., Boiko A., Bykova O., Waubant E., Mah J.K., Stoian C., Kremenchutzky M., Bardini M.R., Ruggieri M., Rensel M., Hahn J., Weinstock-Guttman B., Yeh E.A., Farrell K., Freedman M., Iivanainen M., Sevon M., Bhan V., Dilenge M.E., Stephens D., Bar-Or A. Clinical features and viral serologies in children with multiple sclerosis a multinational observational study. Lancet Neurol. 2007;6:773-781.

    Not in our library10.1016/s1474-4422(07)70196-5 (opens in a new tab)

  112. 112.

    Sekigawa I., Nawata M., Seta N., Yamada M., Iida N., Hashimoto H. Cytomegalovirus infection in patients with systemic lupus erythematosus. Clin. Exp. Rheumatol. 2002;20:559-564.

    Not in our library

  113. 113.

    Hrycek A., Kusmierz D., Mazurek U., Wilczok T. Human cytomegalovirus in patients with systemic lupus erythematosus. Autoimmunity. 2005;38:487-491.

    Not in our library10.1080/08916930500285667 (opens in a new tab)

  114. 114.

    Zivadinov R., Nasuelli D., Tommasi M.A., Serafin M., Bratina A., Ukmar M., Pirko I., Johnson A.J., Furlan C., Pozzi-Mucelli R.S., Monti-Bragadin L., Grop A., Zambon M., Antonello R.M., Cazzato G., Zorzon M. Positivity of cytomegalovirus antibodies predicts a better clinical and radiological outcome in multiple sclerosis patients. Neurol. Res. 2006;28:262-269.

    Not in our library10.1179/016164106x98134 (opens in a new tab)

  115. 115.

    Fotheringham J., Jacobson S. Human herpesvirus 6 and multiple sclerosis potential mechanisms for virus-induced disease. Herpes. 2005;12:4-9.

    Not in our library

  116. 116.

    Rotola A., Merlotti I., Caniatti L., Caselli E., Granieri E., Tola M.R., Di Luca D., Cassai E. Human herpesvirus 6 infects the central nervous system of multiple sclerosis patients in the early stages of the disease. Mult. Scler. 2004;10:348-354.

    Not in our library10.1191/1352458504ms1045oa (opens in a new tab)

  117. 117.

    Boucher A., Desforges M., Duquette P., Talbot P.J. Long-term human coronavirus-myelin cross-reactive T-cell clones derived from multiple sclerosis patients. Clin. Immunol. 2007;123:258-267.

    Not in our library10.1016/j.clim.2007.02.002 (opens in a new tab)

  118. 118.

    Schweizer M., Turek R., Reinhardt M., Neumann-Haefelin D. Absence of foamy virus DNA in Graves' disease. AIDS Res. Hum. Retroviruses. 1994;10:601-605.

    Not in our library10.1089/aid.1994.10.601 (opens in a new tab)

  119. 119.

    Wick G., Trieb K., Aguzzi A., Recheis H., Anderl H., Grubeck-Loebenstein B. Possible role of human foamy virus in Graves' disease. Intervirology. 1993;35:101-107.

    Not in our library10.1159/000150300 (opens in a new tab)

  120. 120.

    Sun K.H., Lin H.Y., Chen L.W., Tai H.Y., Lin M.L., Feng C.K., Sung J.S., Liu H.F., Liu W.T. Human foamy virus bel1 sequence in patients with autoimmune rheumatic diseases. Clin. Rheumatol. 2006;25:694-699.

    Not in our library10.1007/s10067-005-0146-5 (opens in a new tab)

  121. 121.

    Saib A., Canivet M., Giron M.L., Bolgert F., Valla J., Lagaye S., Peries J., de The H. Human foamy virus infection in myasthenia gravis. Lancet. 1994;343:666.

    Not in our library10.1016/s0140-6736(94)92657-3 (opens in a new tab)

  122. 122.

    Sekigawa I., Kaneko H., Hishikawa T., Hashimoto H., Hirose S., Kaneko Y., Maruyama N. HIV infection and SLE: their pathogenic relationship. Clin. Exp. Rheumatol. 1998;16:175-180.

    Not in our library

  123. 123.

    Maradona J.A., Carton J.A., Asensi V. Myasthenia gravis and systemic lupus erythematosus in association with human immunodeficiency virus infection. Clin. Infect. Dis. 1995;20:1577-1578.

    Not in our library10.1093/clinids/20.6.1577 (opens in a new tab)

  124. 124.

    Matsuda T., Tomita M., Uchihara J.N., Okudaira T., Ohshiro K., Tomoyose T., Ikema T., Masuda M., Saito M., Osame M., Takasu N., Ohta T., Mori N., Human T. cell leukemia virus type I-infected patients with Hashimoto's thyroiditis and Graves' disease. J. Clin. Endocrinol. Metab. 2005;90:5704-5710.

    Not in our library10.1210/jc.2005-0679 (opens in a new tab)

  125. 125.

    Kubonishi I., Kubota T., Sawada T., Tanaka Y., Machida H., Yoshida O., Fukushima A., Ueno H., Ohtsuki Y., Miyoshi I. An HTLV-I carrier with Graves' disease followed by uveitis isolation of HTLV-I from thyroid tissue. Int. J. Hematol. 1997;66:233-237.

    Not in our library10.1016/s0925-5710(97)00595-1 (opens in a new tab)

  126. 126.

    Akimoto M., Matsushita K., Suruga Y., Aoki N., Ozaki A., Uozumi K., Tei C., Arima N. Clinical manifestations of human T lymphotropic virus type I-infected patients with systemic lupus erythematosus. J. Rheumatol. 2007;34:1841-1848.

    Not in our library

  127. 127.

    Alvarez-Lafuente R., Garcia-Montojo M., De Las Heras V., Bartolome M., Arroyo R. JC virus in cerebrospinal fluid samples of multiple sclerosis patients at the first demyelinating event. Mult. Scler. 2007;13:590-595.

    Not in our library10.1177/1352458506073116 (opens in a new tab)

  128. 128.

    Franciotta D., Bestetti A., Bergamaschi R., Piccolo G., Persico A., Cinque P. Failure to detect JC virus DNA in cerebrospinal fluid of multiple sclerosis patients. Mult. Scler. 2006;12:674-675.

    Not in our library10.1177/1352458506070635 (opens in a new tab)

  129. 129.

    Du Pasquier R.A., Stein M.C., Lima M.A., Dang X., Jean-Jacques J., Zheng Y., Letvin N.L., Koralnik IJ J.C. virus induces a vigorous CD8+ cytotoxic T cell response in multiple sclerosis patients. J. Neuroimmunol. 2006;176:181-186.

    Not in our library10.1016/j.jneuroim.2006.04.003 (opens in a new tab)

  130. 130.

    Mori K., Munakata Y., Saito T., Tani J., Nakagawa Y., Hoshikawa S., Ozaki H., Ito S., Yoshida K. Intrathyroidal persistence of human parvovirus B19 DNA in a patient with Hashimoto's thyroiditis. J. Infect. 2007;55:e29-31.

    Not in our library10.1016/j.jinf.2007.05.173 (opens in a new tab)

  131. 131.

    Chen Y.S., Chou P.H., Li S.N., Tsai W.C., Lin K.H., Tsai K.B., Yen J.H., Liu H.W. Parvovirus B19 infection in patients with rheumatoid arthritis in Taiwan. J. Rheumatol. 2006;33:887-891.

    Not in our library

  132. 132.

    Munakata Y., Kodera T., Saito T., Sasaki T. Rheumatoid arthritis, type 1 diabetes, and Graves' disease after acute parvovirus B19 infection. Lancet. 2005;366:780.

    Not in our library10.1016/s0140-6736(05)67184-x (opens in a new tab)

  133. 133.

    O'Brayan T.A., Beck M.J., Demers L.M., Naides S.J. Human parvovirus B19 infection in children with new onset Type 1 diabetes mellitus. Diabet. Med. 2005;22:1778-1779.

    Not in our library10.1111/j.1464-5491.2005.01708.x (opens in a new tab)

  134. 134.

    Caliskan R., Masatlioglu S., Aslan M., Altun S., Saribas S., Ergin S., Uckan E., Koksal V., Oz V., Altas K., Fresko I., Kocazeybek B. The relationship between arthritis and human parvovirus B19 infection. Rheumatol. Int. 2005;26:7-11.

    Not in our library10.1007/s00296-004-0494-5 (opens in a new tab)

  135. 135.

    Koenigbauer U.F., Eastlund T., Day J.W. Clinical illness due to parvovirus B19 infection after infusion of solvent/detergent-treated pooled plasma. Transfusion. 2000;40:1203-1206.

    Not in our library10.1046/j.1537-2995.2000.40101203.x (opens in a new tab)

  136. 136.

    Makela M., Oling V., Marttila J., Waris M., Knip M., Simell O., Ilonen J. Rotavirus-specific T cell responses and cytokine mRNA expression in children with diabetes-associated autoantibodies and type 1 diabetes. Clin. Exp. Immunol. 2006;145:261-270.

    Not in our library10.1111/j.1365-2249.2006.03146.x (opens in a new tab)

  137. 137.

    Gergely P. Jr., Perl A., Poor G. Possible pathogenic nature of the recently discovered TT virus does it play a role in autoimmune rheumatic diseases? Autoimmun. Rev. 2006;6:5-9.

    Not in our library10.1016/j.autrev.2006.03.002 (opens in a new tab)

  138. 138.

    Kilding R., Iles M.M., Timms J.M., Worthington J., Wilson A.G. Additional genetic susceptibility for rheumatoid arthritis telomeric of the DRB1 locus. Arthritis. Rheum. 2004;50:763-769.

    Not in our library10.1002/art.20043 (opens in a new tab)

  139. 139.

    Okamoto K., Makino S., Yoshikawa Y., Takaki A., Nagatsuka Y., Ota M., Tamiya G., Kimura A., Bahram S., Inoko H. Identification of I kappa BL as the second major histocompatibility complex-linked susceptibility locus for rheumatoid arthritis. Am. J. Hum. Genet. 2003;72:303-312.

    Not in our library10.1086/346067 (opens in a new tab)

  140. 140.

    Singal D.P., Li J., Lei K. Genetics of rheumatoid arthritis (RA): two separate regions in the major histocompatibility complex contribute to susceptibility to RA. Immunol. Lett. 1999;69:301-306.

    Not in our library10.1016/s0165-2478(99)00108-x (opens in a new tab)

  141. 141.

    Simmonds M.J., Heward J.M., Barrett J.C., Franklyn J.A., Gough S.C. Association of the BTNL2 rs2076530 single nucleotide polymorphism with Graves' disease appears to be secondary to DRB1 exon 2 position beta74. Clin. Endocrinol. (Oxf). 2006;65:429-432.

    Not in our library10.1111/j.1365-2265.2006.02586.x (opens in a new tab)

  142. 142.

    Yang Y., Chung E.K., Wu Y.L., Savelli S.L., Nagaraja H.N., Zhou B., Hebert M., Jones K.N., Shu Y., Kitzmiller K., Blanchong C.A., McBride K.L., Higgins G.C., Rennebohm R.M., Rice R.R., Hackshaw K.V., Roubey R.A., Grossman J.M., Tsao B.P., Birmingham D.J., Rovin B.H., Hebert L.A., Yu C.Y. Gene copy-number variation and associated polymorphisms of complement component C4 in human systemic lupus erythematosus (SLE) low copy number is a risk factor for and high copy number is a protective factor against SLE susceptibility in European Americans. Am. J. Hum. Genet. 2007;80:1037-1054.

    Not in our library10.1086/518257 (opens in a new tab)

  143. 143.

    Hauptmann G., Grosshans E., Heid E. Lupus erythematosus syndrome and complete deficiency of the fourth component of complement. Boll. Ist. Sieroter. Milan. 1974;53(suppl: 228).

    Not in our library

  144. 144.

    Lewis M.J., Botto M. Complement deficiencies in humans and animals: links to autoimmunity. Autoimmunity. 2006;39:367-378.

    Not in our library10.1080/08916930600739233 (opens in a new tab)

  145. 145.

    Wu Y.L., Higgins G.C., Rennebohm R.M., Chung E.K., Yang Y., Zhou B., Nagaraja H.N., Birmingham D.J., Rovin B.H., Hebert L.A., Yu C.Y. Three distinct profiles of serum complement C4 proteins in pediatric systemic lupus erythematosus (SLE) patients: tight associations of complement C4 and C3 protein levels in SLE but not in healthy subjects. Adv. Exp. Med. Biol. 2006;586:227-247.

    Not in our library10.1007/0-387-34134-x_16 (opens in a new tab)

  146. 146.

    Yang Y., Chung E.K., Zhou B., Lhotta K., Hebert L.A., Birmingham D.J., Rovin B.H., Yu C.Y. The intricate role of complement component C4 in human systemic lupus erythematosus. Curr. Dir. Autoimmun. 2004;7:98-132.

    Not in our library10.1159/000075689 (opens in a new tab)

  147. 147.

    Stone N.M., Williams A., Wilkinson J.D., Bird G. Systemic lupus erythematosus with C1q deficiency. Br. J. Dermatol. 2000;142:521-524.

    Not in our library10.1046/j.1365-2133.2000.03369.x (opens in a new tab)

  148. 148.

    Pickering M.C., Walport M.J. Links between complement abnormalities and systemic lupus erythematosus. Rheumatology (Oxford). 2000;39:133-141.

    Not in our library10.1093/rheumatology/39.2.133 (opens in a new tab)

  149. 149.

    Tsao B.P. The genetics of human systemic lupus erythematosus. Trends Immunol. 2003;24:595-602.

    Not in our library10.1016/j.it.2003.09.006 (opens in a new tab)

  150. 150.

    Lee Y.J., Huang F.Y., Wang C.H., Lo F.S., Tsan K.W., Hsu C.H., Huang C.Y., Chang S.C., Chang J.G. Polymorphism in the transmembrane region of the MICA gene and type 1 diabetes. J. Pediatr. Endocrinol. Metab. 2000;13:489-496.

    Not in our library10.1515/jpem.2000.13.5.489 (opens in a new tab)

  151. 151.

    Kawabata Y., Ikegami H., Kawaguchi Y., Fujisawa T., Hotta M., Ueda H., Shintani M., Nojima K., Ono M., Nishino M., Taniguchi H., Noso S., Yamada K., Babaya N., Ogihara T. Age-related association of MHC class I chain-related gene A (MICA) with type 1 (insulin-dependent) diabetes mellitus. Hum. Immunol. 2000;61:624-629.

    Not in our library10.1016/s0198-8859(00)00118-x (opens in a new tab)

  152. 152.

    Park Y., Lee H., Sanjeevi C.B., Eisenbarth G.S. MICA polymorphism is associated with type 1 diabetes in the Korean population. Diabetes Care. 2001;24:33-38.

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