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Zinc Status and Autoimmunity: A Systematic Review and Meta-Analysis

Alessandro Sanna, Davide Firinu, Patrizia Zavattari and 1 more

Nutrients · 2018 · Meta-analysis · CC BY

doi:10.3390/nu10010068

Abstract

Zinc is an essential trace element for living organisms and their biological processes. Zinc plays a key role in more than 300 enzymes and it is involved in cell communication, proliferation, differentiation and survival. Zinc plays also a role in regulating the immune system with implications in pathologies where zinc deficiency and inflammation are observed. In order to examine the experimental evidence reported in the literature regarding zinc levels in the body of patients with autoimmune disorders compared to control individuals, a systematic review and meta-analysis were performed. From 26,095 articles identified by literature search, only 179 of them were considered potentially relevant for our study and then examined. Of the 179 articles, only 62 satisfied the inclusion criteria. Particularly for Fixed Model, Zn concentration in both serum (mean effect = −1.19; confidence interval: −1.26 to −1.11) and plasma (mean effect = −3.97; confidence interval: −4.08 to −3.87) samples of autoimmune disease patients was significantly lower than in controls. The data presented in our work, although very heterogeneous in the manner of collecting and investigating samples, have proved to be extremely consistent in witnessing a deficiency of zinc in serum and plasma of patients compared to controls.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 26, 2026. Paragraph numbers are ours, so an answer can point at one.

1. Introduction

Zinc is an essential trace element for living organisms and their biological processes. The body cannot accumulate zinc and it is, therefore, essential to take this element consistently in the diet. Although dietary zinc levels vary substantially, eukaryotic cells need to maintain intracellular zinc homeostasis to ensure its proper function. This homeostasis is regulated in mammals by import and export processes, vesicle retaining zinc (zincosomes) and association to metallothioneins (MTs). Zinc plays a key structural or catalytic role in more than 300 enzymes and is involved at all levels of cellular signal transduction. Zinc is involved in cell communication, cell proliferation, differentiation and survival. Therefore, zinc also plays a key role in regulating the immune system, both innate and adaptive, with consequent implications in pathologies where zinc deficiency and inflammation are observed.

The understanding of zinc’s importance in human health unfortunately begun only in the 1960s. Zinc deficiency is associated with a decline in the immune system, with inflammation leading to chronicity. In addition, dietary zinc deficiency was considered to be very rare, although it affects 20–25% of the world’s population. Data from the World Health Organization report that zinc deficiency is the fifth largest health risk factor in developing countries and the eleventh in the world. Rarely is zinc deficiency seen as a serious deficit; more frequently it is seen as a less accentuated deficit. Patients with severe deficits present: lymphopenia, decreased ratio between T helper (Th) to cytotoxic T cells, reduced natural killer (NK) cell activity, and increased monocytes cytotoxicity. This condition characterizes the malabsorption autosomal recessive syndrome, Acrodermatitis enteropathica, due to a mutation of a zinc-importing protein, ZIP4.

Less accentuated zinc deficiency states can be caused by nutritional deficits due, for example, to a diet high in lignin and phytates, in vegetarians and vegans, chelating zinc, so preventing its proper absorption. This state is characterized by slight weight loss, rough skin, oligospermia and hyperammoniaemia.

Several clinical trials of zinc supplementation have been conducted in patients with zinc deficit suffering from various pathologies (viral, bacterial and parasitic infections or autoimmune diseases), or as vaccine supplements. Although there is countless evidence supporting the fact that controlled zinc supplementation can prevent chronic inflammation and other zinc deficiency-related illnesses, or even improve symptoms (as seen in both humans and animal models), to date zinc supplementation does not fall into commonly used medical practices in risk subjects/populations. The purpose of this study was to examine the experimental evidence reported in the literature over the last 40 years regarding zinc levels in the body of patients with autoimmune disorders compared to control individuals. The biological matrices for which it was possible to collect enough bibliographic material to perform a meta-analysis were predominantly serum and plasma; to a lesser extent data were collected on urine, hair and spinal fluid.

2.1. Search Strategy

In order to select the included studies, a literature search was undertaken of PubMed, Cochrane Central Register of Controlled Trials, Web of Science and Science Direct databases from inception to 23 January 2017 and without any limitation of on year of publication. Keywords used were zinc and ((dietary or supplement) or (serum or plasma)) and (autoimmune disease or autoimmunity). Typing, in the search window, the keywords in the databases chosen, without any restrictions, the result was a list of publications for which only the title, authors and abstracts were available. After eliminating the duplicates the titles and abstracts of the remaining articles were read and those not relevant for the purpose of this meta-analysis were excluded. After this step, the entire manuscript of each remaining paper, defined as eligible, was read, thus excluding those that did not fall within the criteria defined in the “study eligibility criteria” (Section 2.3, below). Finally, the papers that satisfied all selection criteria have been included in the meta-analysis.

Full search details for all databases are presented in Table S1 (Supplemental Material). This study was performed according to Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) requirements. The standard flowchart, which describes the process selection, is reported in Figure 1.

2.2. Study Selection

All reference lists were downloaded for elimination of duplicates. Furthermore, title and abstract of each reference were screened by two independent reviewers to perform the eligibility assessment of full text for this review. Study eligibility was restricted to human studies and English language.

2.3. Study Eligibility Criteria

Observational studies, prospective and retrospective studies, case-control studies or randomized controlled trials (RCTs) investigating the relationship between zinc status and autoimmune diseases were eligible for inclusion. In particular, only diseases for which the autoimmunity was a franc condition were included in this study. The American Autoimmune Related Diseases Association (AARDA) was consulted to verify that the diseases considered in this study were really autoimmune diseases.

The studies were selected if zinc concentration in biological samples or dietary/supplemental zinc were an index of zinc status.

Moreover, the presence of both number of subject involved (≥5) and the statistical parameters were taken into account for the meta-analysis process. On the other hand, letters, conference proceedings, reviews, duplicated data, data of both animal and cellular studies, and studies that did not indicate data of interest were excluded. Although studies on animals are not considered eligible for the meta-analysis process, a discussion on them was performed separately. Also, thirteen studies were excluded because we did not have access to the full text, maybe the most of these studies were published more than 20 years ago.

2.4. Study Quality Assessment and Data Extraction

The Newcastle-Ottawa Scale (NOS) for case-control studies was used to assess the quality of the included studies. Ten full-text studies were excluded because control data was not complete in reference to both number of controls and their relationship with cases. Two independent reviewers extracted data from each eligible study. The data extracted included the type of study (observational studies, prospective and retrospective studies, case-control studies, randomized controlled trials), country, year of publication, sample size, age and sex of patients, autoimmune disease, zinc status in biological samples, type of samples, method of samples analysis, statistical method, standard deviation and statistical significance.

Table 1 reports the general characteristics of selected studies included in meta-analysis in reference to serum samples whereas Table 2 indicates the baseline characteristics for meta-analysis related to plasma samples. Furthermore, Table 3 reports the general information about the studies that are related to hair, urine and Cerebral Spinal Fluid (CSF) samples.

In most of the included studies, the measurement unit of the zinc concentration data were different for the same biological media. For this reason, all data of zinc in both serum and plasma samples were converted in μg/mL, whereas zinc data in hair samples were converted in μg/g.

2.5. Statistical Analysis

Data were processed by MetaEasy Excel add-in (Microsoft Corporation, Redmond, WA, USA), which used seven different methods. In particular, three methods refer to dichotomous data and four methods refer to continuous data. In order to improve their heterogeneity, data were grouped depending on different biological media: serum, plasma, hair, urine and cerebrospinal fluid. Means of zinc status in both patients and controls, standard deviations of zinc status in both patients and controls, number of subjects involved and p-value were used. p-value < 0.05 was considered as statistically significant.

Also, overall estimates of effect were performed with seven models: Fixed Effects (FE), DerSimonial-Laird (DL), Q method (Q), Maximum-Likelihood (ML), Profile—Likelihood (PL), t-Test (T) and Permutations method (PE). Heterogeneity was assessed by different measures: Cochrane’s Q, τ2 test, I2 test and H2M test. Publication bias was evaluated using funnel plot 3 considering the estimate of effects and their standard errors as a precision indicator (1/SE).

3. Results

From 26,095 articles identified by literature search, 21,766 duplicates were deleted. After the screening of 4329 remaining articles, 4150 of them were excluded because they were irrelevant for our study. Afterwards, 179 papers were considered potentially relevant for our study but only 62 of them satisfied the inclusion criteria (see Section 2.4). Therefore, 117 articles were excluded and the reasons for their exclusion is shown in PRISMA diagram (Figure 1). In particular, 13 of the 117 papers were excluded because, with the means available to the Italian library system, it was not possible to retrieve them. However, the 13 papers are listed in Table S2 (Supplemental Material).

3.1. Zn Status and Autoimmune Diseases

The relationship between Zn status and autoimmune diseases has been investigated by many authors since the 1970s. The 62 studies included in the meta-analysis were case-control studies. Also, all of them were published between 1975 and 2017 and they are related to different autoimmune diseases. Indeed, 22 studies describe the zinc status in Type 1 Diabetes (T1D), 18 full-text are related to Rheumatoid Arthritis (RA), 7 articles investigated zinc status in Multiple Sclerosis (MS) patients while 15 papers are related to other diseases among which Alopecia Areata (AA), Systemic Lupus Erythematosus (SLE), Pemphigus Vulgaris (PV), Autoimmune Hepatitis (AH), Celiac Disease (CD), Hashimoto Thyroiditis (HT), Sjogren’s syndrome (SS), Juvenile Idiopathic Arthritis (JIA).

3.2. Zn Status in Serum Samples

The meta-analysis results show that, for all models, Zn concentration in serum of autoimmune disease patients was significantly lower than controls (FE: mean effect = −1.19 and confidence interval: −1.26 to −1.11; DL: mean effect = −1.29 and confidence interval: −1.91 to −0.67; Q: mean effect = −1.29 and confidence interval: −1.91 to −0.67; ML: mean effect = −1.29 and confidence interval: −1.96 to −0.63; PL: mean effect = −1.29 and confidence interval: −1.97 to −0.61; T: mean effect = −1.29 and confidence interval: −1.99 to −0.60; PE: mean effect = −1.29 and confidence interval: −2.95 to −0.49). Indeed, 70% of the articles considered show that patients have a zinc deficiency compared to the control group.

Regarding the heterogeneity of data, the elaboration shows the following results: Cochrane Q = 2589.53; τ2 = 3.88 (for DL model); τ2 = 4.52 (for ML and PL models); I2 = 98.49%; H2M = 65.39. Forest plot in Figure 2 shows the study effects for each study and the overall estimates effects. Despite high heterogeneity, overall estimates effects were positive for all models. Moreover, overall effects that were calculated with FE models were more efficient than effects calculated with the other models.

3.3. Zn Status in Plasma Samples

As already seen for serum, also in plasma samples the meta-analysis results show that, for all models, Zn concentration in the serum of autoimmune disease patients was significantly lower than controls. Indeed, for 62% of the articles included in the meta-analysis process, patients had lower zinc concentrations than controls.

As shown in Figure 3, only FE model overall estimates effects could be considered favorable (FE: mean effect = −3.97 and confidence interval: −4.08 to −3.87). Even in this case, as in the previous one, data was highly heterogeneous.

3.4. Zn Status in Hair, Urine and Cerebrospinal Fluid Samples

In reference to Zn hair concentration, only FE model overall estimates effects could be considered favorable (FE: mean effect = −2.49 and confidence interval: −2.72 to −2.28). However, heterogeneity was considerable and the number of studies was limited. On the other hand, no significant variations in urinary and CSF zinc were observed between patients and controls.

3.5. Publication Bias

To evaluate the presence of publication bias, Funnel Plots were calculated. As shown in Figure 4, in both meta-analysis related to serum Zn and plasma Zn, it is possible to observe the presence of bias in the selected literature.

4. Discussion

This review of the literature on the possible linkage between zinc levels (especially in serum and plasma) and autoimmune diseases has revealed a huge amount of studies on this subject, although the selection due to meta-analysis methods has narrowed the final analysis to 62 publications, temporally distributed as shown in Figure S1 (Supplemental Material).

As expected, the data presented in this review, although very heterogeneous in the manner of collecting and investigating samples, etc., have proved to be extremely consistent in witnessing a deficiency of zinc in serum and plasma of patients compared to controls. A recurring question found in many studies was whether alterations in the homeostasis of this element represent the basis of the inflammatory status or consequences thereof.

As is well known, there are populations such as Finnish or Sardinian with polygenic predisposition to autoimmune diseases, in whom there has been a natural selection in favor of certain genetic loci, playing a role in the immune response. In particular, certain HLA (Humane Leucocyte Antigens) haplotypes, such as HLA-DR3-B18 in Sardinia and HLA-DR4 in Finland, are particularly frequent in those populations, terribly increasing the relative risk of developing multiple sclerosis, type 1 diabetes and even comorbidity of these two and other autoimmune pathologies. In addition, recent works have also shown that DNA genetic variations largely drive the development and function of specific leukocyte subsets, in particular those who may have key pro-inflammatory or regulatory roles in autoimmune diseases.

Of note, there is the repeated observation of a sex-related bias in different autoimmune diseases, but often not attributable to known genetic causes, and that environmental influences at various timepoints contribute to a shift towards unbalanced immune responses.

Zinc has been recognized as one of these factors, as its homeostasis is essential against inflammatory diseases to regulate different aspects of the immune system, both for innate and adaptive immune response, cell cycle progression, cell maturation and differentiation. Zinc deficiency is therefore associated with an incorrect maturation and function of T and B cells, an unbalanced ratio between Th1 and Th2, and between regulatory and pro-inflammatory T cells, and a weakening of NK cell function. Zinc can inhibit Th17 lymphocytes, which confer susceptibility to autoimmune diseases owing to their strong inflammatory properties, as well as a variety of other proinflammatory responses on T-cells and B-cells.

These unbalanced states can, however, be restored by zinc integration. As demonstrated in several studies analyzed in this meta-analysis, patients with multiple sclerosis exhibit low levels of zinc in the plasma. This is also observed in the mouse model, affected by experimental autoimmune encephalomyelitis (EAE), in which the symptoms decrease in severity and even regress after zinc treatment, inducing proliferation of regulatory T cells and decreasing pro-inflammatory cells. Even in type 1 diabetes, the autoimmune diabetes, zinc homeostasis plays a key role by acting on various molecular mechanisms. The protagonist in beta-pancreatic cells is definitely the ZnT8 zinc importer, essential for the transport of insulin secretory vesicles, and for the formation of insulin granules. Even in this case, the benefits of zinc supplementation are known. Chronic zinc deficiency increases inflammation potentially leading to its chronic perpetuation.

Alternatively, hypozincemia could represent a common result of inflammation during the autoimmune disorders here discussed. It has been shown that induction of acute-phase response upregulates Zip14 via IL-6 and IL-1 signaling, inducing liver sequestration and redistribution in the cellular compartment. Furthermore, the experiments conducted by Bonaventura and colleagues on synovial cells isolated from joints of patients affected by rheumatoid arthritis are illuminating. The authors have shown that exposure of cells to pro-inflammatory cytokines such as interleukin-17 and tumor necrosis factor alpha, increases the expression of zinc importer carriers, resulting in enhanced intracellular Zn uptake and further increasing inflammation and interleukin-6 production. These experiments have clarified the existence of a feedback loop between inflammation and cellular zinc uptake.

Indeed, in pathologies such as multiple sclerosis, serum levels of zinc decrease mainly during relapses; in pathologies characterized by chronic inflammation, such as rheumatoid arthritis, a continuous recruitment of zinc within the cells would be established, hence a continuous depletion of zinc in serum. Probably, in the induction of autoimmunity, there is a role for either a primary zinc deficiency and for its secondary reduction due to inflammation, that warrant further focused studies for a thorough determination of timing (preclinical phase of disease vs. overt disease or during pregnancy, childhood, and elderly), cause/pathophysiology, degree of reduction and span/duration (over time) of hypozincemia. Finally, zinc also acts as a co-factor for many proteins implicated in the epigenome establishment. This means that the development of a new organism may be conditioned, from the earliest stages, by possible imbalance in zinc homeostasis. Therefore, interventions to correct any nutritional imbalances should be anticipated during the stages of pregnancy and lactation. In fact, zinc deficiencies during pregnancy are associated with fetal or adult illness, also due to the improper development of the immune system.

One aspect not to be overlooked is the bioaccessibility and then the bioavailability of this and other elements. In this regard, environmental studies are also desirable for helping to clarify the potential environmental impact of exposures/deficiencies to particular elements, essential for/toxic to human health, including any corrective measures to improve the conditions in which man lives and works and therefore having a strong impact on human health. In fact, in the mining exploration field, it is well known that the abundance of some elements is typically linked to some lithologies and/or metallogenic contexts. This relative abundance (or deficiency) affects any media linked to these environments such as water, soil and so also the biological sphere. However, it should be considered that the complexity and dynamism of the environment could complicate the interpretations.

Given the importance of zinc in regulating the functioning of the immune system, it is, therefore, logical to associate an imbalance in the homeostasis of this element with the state of autoimmunity. It would therefore be desirable to mount a screening campaign for the evaluation of zinc levels in neonatal, preschool and school-age children, and hence a relevant campaign for the integration of essential elements for man, including zinc. In populations at higher genetic risk of autoimmunity it would be therefore interesting to have a clinical trial investigate personalized zinc supplementation for preventing and/or treating autoimmune diseases.

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  50. 50.

    Nicoloff G., Angelova M., Nikolov A. Serum fibrillin-antifibrillin immune complexes among diabetic children. Vascul. Pharmacol. 2005;43:171-175.

    Not in our library10.1016/j.vph.2005.06.005

  51. 51.

    Önal S., Nazıroğlu M., Çolakm M., Bulut V., Flores-Arce M.F. Effects of different medical treatments on serum copper, selenium and zinc levels in patients with rheumatoid arthritis. Biol. Trace Elem. Res. 2011;142:447-455.

    Not in our library10.1007/s12011-010-8826-7

  52. 52.

    Palm R., Hallmans G. Zinc and copper in multiple sclerosis. J. Neurol. Neurosurg. Psychiatry. 1982;45:691-698.

    Not in our library10.1136/jnnp.45.8.691

  53. 53.

    Raz I., Havivi E. Trace elements in blood cells of diabetic subjects. Diabetes Res. 1989;10:21-24.

    Not in our library

  54. 54.

    Sahebari M., Abrishami-Moghaddam M., Moezzi A., Ghayour-Mobarhan M., Mirfeizi Z., Esmaily H., Ferns G. Association between serum trace element concentrations and the disease activity of systemic lupus erythematosus. Lupus. 2014;23:793-801.

    Not in our library10.1177/0961203314530792

  55. 55.

    Silverio Amancio O.M., Alves Chaud D.M., Yanaguibashi G., Esteves Hilário M.O. Copper and zinc intake and serum levels in patients with juvenile rheumatoid arthritis. Eur. J. Clin. Nutr. 2003;57:706-712.

    Not in our library10.1038/sj.ejcn.1601601

  56. 56.

    Ullah Z., Ullah M.I., Hussain S., Kaul H., Lone K.P. Determination of Serum Trace Elements (Zn, Cu, and Fe) in Pakistani Patients with Rheumatoid Arthritis. Biol. Trace Elem. Res. 2017;175:10-16.

    Not in our library10.1007/s12011-016-0746-8

  57. 57.

    Yazdanpanah M.P., Ghayour-Mobarhan M., Taji A., Javidi Z., Pezeshkpoor F., Tavallaie S., Momenzadeh A., Esmaili H., Shojaie-Noori S., Khoddami M., et al. Serum zinc and copper status in Iranian patients with pemphigus vulgaris. Int. J. Dermatol. 2011;50:1343-1346.

    Not in our library10.1111/j.1365-4632.2011.04968.x

  58. 58.

    Yilmaz A., Sari R.A., Gundogdu M., Kose N., Dag E. Trace elements and some extracellular antioxidant proteins levels in serum of patients with systemic lupus erythematosus. Clin. Rheumatol. 2005;24:331-335.

    Not in our library10.1007/s10067-004-1028-y

  59. 59.

    Zoli A., Altomonte L., Caricchio R., Galossi A., Mirone L., Ruffini M.P., Magaró M. Serum zinc and copper in active rheumatoid arthritis: Correlation with interleukin 1 beta and tumour necrosis factor alpha. Clin. Rheumatol. 1998;17:378-382.

    Not in our library10.1007/bf01450895

  60. 60.

    Arreola F., Paniagua R., Herrera J., Díaz-Bensussen S., Mondragón L., Bermúdez J.A., Pérez Pastén E., Villalpando S. Low plasma zinc and androgen in insulin-dependent diabetes mellitus. Arch. Androl. 1986;16:151-154.

    Not in our library10.3109/01485018608986935

  61. 61.

    Bacon M.C., White P.H., Raiten D.J., Craft N., Margolis S., Levanderh O.A., Taylor M.L., Lipnick R.N., Sami S. Nutritional status and growth in juvenile heumatoid arthritis. Semin. Arthritis Rheum. 1990;20:97-106.

    Not in our library10.1016/0049-0172(90)90022-8

  62. 62.

    Balogh Z., El-Ghobarey A.F., Fell G.S., Brown D.H., Dunlop J., Dick W.C. Plasma zinc and its relationship to clinical symptoms and drug treatment in rheumatoid arthritis. Ann. Rheum. Dis. 1980;39:329-332.

    Not in our library10.1136/ard.39.4.329

  63. 63.

    Crofton R.W., Glover S.C., Ewen S.W., Aggett P.J., Mowat N.A., Mills C.F. Zinc absorption in celiac disease and dermatitis herpetiformis: A test of small intestinal function. Am. J. Clin. Nutr. 1983;38:706-712.

    Not in our library10.1093/ajcn/38.5.706

  64. 64.

    Cunningham J.J., Fu A., Mearkle P.L., Brown G. Hyperzincuria in individuals with insulin-dependent diabetes mellitus: Concurrent zinc status and the effect of high-dose zinc supplementation. Metabolism. 1994;43:1558-1562.

    Not in our library10.1016/0026-0495(94)90016-7

  65. 65.

    Ho S.Y., Catalanotto F.A., Lisak R.P., Dore-Duffy P. Zinc in multiple sclerosis. II: Correlation with disease activity and elevated plasma membrane-bound zinc in erythrocytes from patients with multiple sclerosis. Ann. Neurol. 1986;20:712-715.

    Not in our library10.1002/ana.410200610

  66. 66.

    Kennedy A.C., Fell G.S., Rooney P.J., Stevens W.H., Dick W.C., Buchanan W.W. Zinc: Its relationship to osteoporosis in rheumatoid arthritis. Scand. J. Rheumatol. 1975;4:243-245.

    Not in our library10.3109/03009747509165264

  67. 67.

    Melchior T., Wiese Simonsen A., Johannessen C., Binder C. Plasma zinc concentrations during the first 2 years after diagnosis of insulin-dependent diabetes mellitus: A prospective study. J. Intern. Med. 1989;226:53-58.

    Not in our library10.1111/j.1365-2796.1989.tb01353.x

  68. 68.

    Milanino R., Frigo A., Bambara L.M., Marrella M., Moretti U., Pasqualicchio M., Biasi D., Gasperini R., Mainenti L., Velo G.P. Copper and zinc status in rheumatoid arthritis: Studies of plasma, erythrocytes, and urine, and their relationship to disease activity markers and pharmacological treatment. Clin. Exp. Rheumatol. 1993;11:271-281.

    Not in our library

  69. 69.

    Mocchegiani E., Boemi M., Fumelli P., Fabris N. Zinc-dependent low thymic hormone level in type I diabetes. Diabetes. 1989;38:932-937.

    Not in our library10.2337/diab.38.7.932

  70. 70.

    Naveh Y., Schapira D., Ravel Y., Geller E., Scharf Y. Zinc metabolism in rheumatoid arthritis: Plasma and urinary zinc and relationship to disease activity. J. Rheumatol. 1997;24:643-646.

    Not in our library

  71. 71.

    Pereira T.C., Saron M.L., Carvalho W.A., Vilela M.M., Hoehr N.F., Hessel G. Research on zinc blood levels and nutritional status in adolescents with autoimmune hepatitis. Arq. Gastroenterol. 2011;48:62-65.

    Not in our library10.1590/s0004-28032011000100013

  72. 72.

    Quilliot D., Dousset B., Guerci B., Dubois F., Drouin P., Ziegler O. Evidence that diabetes mellitus favors impaired metabolism of zinc, copper, and selenium in chronic pancreatitis. Pancreas. 2001;22:299-306.

    Not in our library10.1097/00006676-200104000-00012

  73. 73.

    Rohn R.D., Pleban P., Jenkins L.L. Magnesium, zinc and copper in plasma and blood cellular components in children with IDDM. Clin. Chim. Acta. 1993;215:21-28.

    Not in our library10.1016/0009-8981(93)90245-y

  74. 74.

    Ruíz C., Alegría A., Barberá R., Farré R., Lagarda M.J. Selenium, Zinc and Copper in Plasma of patients with Type 1 Diabetes Mellitus in Different Metabolic Control States. J. Trace Elem. Med. Biol. 1998;12:91-95.

    Not in our library10.1016/s0946-672x(98)80031-x

  75. 75.

    Smith D.K., Feldman E.B., Feldman D.S. Trace element status in multiple sclerosis. Am. J. Clin. Nutr. 1989;50:136-140.

    Not in our library10.1093/ajcn/50.1.136

  76. 76.

    Tuncer S., Kamanli A., Akçil E., Kavas G.O., Seçkin B., Atay M.B. Trace element and magnesium levels and superoxide dismutase activity in rheumatoid arthritis. Biol. Trace Elem. Res. 1999;68:137-142.

    Not in our library10.1007/bf02784402

  77. 77.

    Viktorínová A., Toserová E., Krizko M., Duracková Z. Altered metabolism of copper, zinc, and magnesium is associated with increased levels of glycated hemoglobin in patients with diabetes mellitus. Metabolism. 2009;58:1477-1482.

    Not in our library10.1016/j.metabol.2009.04.035

  78. 78.

    Yazar M., Sarban S., Kocyigit A., Isikan E. Synovial fluid and plasma selenium, copper, zinc, and iron concentrations in patients with rheumatoid arthritis and osteoarthritis. Biol. Trace Elem. Res. 2005;106:123-132.

    Not in our library10.1385/bter:106:2:123

  79. 79.

    Afridi H.I., Kazi T.G., Brabazon D., Naher S. Interaction between zinc, cadmium, and lead in scalp hair samples of Pakistani and Irish smokers rheumatoid arthritis subjects in relation to controls. Biol. Trace Elem. Res. 2012;148:139-147.

    Not in our library10.1007/s12011-012-9352-6

  80. 80.

    Afridi H.I., Talpur F.N., Kazi T.G., Brabazon D. Estimation of toxic elements in the samples of different cigarettes and their effect on the essential elemental status in the biological samples of Irish smoker rheumatoid arthritis consumers. Environ. Monit. Assess. 2015;187:157.

    Not in our library10.1007/s10661-015-4353-5

  81. 81.

    Melø T.M., Larsen C., White L.R., Aasly J., Sjøbakk T.E., Flaten T.P., Sonnewald U., Syversen T. Manganese, copper, and zinc in cerebrospinal fluid from patients with multiple sclerosis. Biol. Trace Elem. Res. 2003;93:1-8.

    Not in our library10.1385/bter:93:1-3:1

  82. 82.

    Peters J.L., Sutton A.J., Jones D.R., Abrams K.R., Rushton L. Contour-enhanced meta-analysis funnel plots help distinguish publication bias from other causes of asymmetry. J. Clin. Epidemiol. 2008;61:991-996.

    Not in our library10.1016/j.jclinepi.2007.11.010

  83. 83.

    Marrosu M.G., Murru R., Murru M.R., Costa G., Zavattari P., Whalen M., Cocco E., Mancosu C., Schirru L., Solla E., et al. 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

  84. 84.

    Zavattari P., Lampis R., Mulargia A., Loddo M., Angius E., Todd J.A., Cucca F. Confirmation of the DRB1-DQB1 loci as the major component of IDDM1 in the isolated founder population of Sardinia. Hum. Mol. Genet. 2000;9:2967-2972.

    Not in our library10.1093/hmg/9.20.2967

  85. 85.
    Genetic loci linked to Type 1 Diabetes and Multiple Sclerosis families in Sardinia · 2008
    Not checked
  86. 86.

    Orrù V., Steri M., Sole G., Sidore C., Virdis F., Dei M., Lai S., Zoledziewska M., Busonero F., Mulas A., et al. Genetic variants regulating immune cell levels in health and disease. Cell. 2013;155:242-256.

    Not in our library10.1016/j.cell.2013.08.041

  87. 87.

    Steri M., Orru V., Idda M.L., Pitzalis M., Pala M., Zara I., Sidore C., Faa V., Floris M., Deiana M., et al. Overexpression of the cytokine BAFF and autoimmunity risk. N. Engl. J. Med. 2017;376:1615-1626.

    Not in our library10.1056/nejmoa1610528

  88. 88.

    Contu D., Morelli L., Zavattari P., Lampis R., Angius E., Frongia P., Murru D., Maioli M., Francalacci P., Todd J.A., et al. Sex-related bias and exclusion mapping of the nonrecombinant portion of chromosome Y in human type 1 diabetes in the isolated founder population of Sardinia. Diabetes. 2002;51:3573-3576.

    Not in our library10.2337/diabetes.51.12.3573

  89. 89.

    Monti M.C., Guido D., Montomoli C., Sardu C., Sanna A., Pretti S., Lorefice L., Marrosu M.G., Valera P., Cocco E. Is Geo-Environmental Exposure a Risk Factor for Multiple Sclerosis? A Population-Based Cross-Sectional Studyin South-Western Sardinia. PLoS ONE. 2016;11:e0163313.

    Not in our library10.1371/journal.pone.0163313

  90. 90.

    Brodin P., Jojic V., Gao T., Bhattacharya S., Angel C.J.L., Furman D., Shen-Orr S., Dekker C.L., Swan G.E., Butte A.J., et al. Variation in the human immune system is largely driven by non-heritable influences. Cell. 2015;160:37-47.

    Not in our library10.1016/j.cell.2014.12.020

  91. 91.

    Wu C., Yosef N., Thalhamer T., Zhu C., Xiao S., Kishi Y., Regev A., Kuchroo V.K. Induction of pathogenic TH 17 cells by inducible salt-sensing kinase SGK1. Nature. 2013;496:513-517.

    Not in our library10.1038/nature11984

  92. 92.

    Haase H., Rink L. Multiple impacts of zinc on immune function. Metallomics. 2014;6:1175-1180.

    Not in our library10.1039/c3mt00353a

  93. 93.

    Prasad A.S. Effects of zinc deficiency on Th1 and Th2 cytokine shifts. J. Infect. Dis. 2000;182:62-68.

    Not in our library10.1086/315916

  94. 94.

    Lee H., Kim B., Choi Y.H., Hwang Y., Kim D.H., Cho S., Hong S.J., Lee W. Inhibition of interleukin-1β-mediated interleukin-1 receptor-associated kinase 4 phosphorylation by zinc leads to repression of memory T helper type 17 response in humans. Immunology. 2015;146:645-656.

    Not in our library10.1111/imm.12536

  95. 95.

    Hojyo S., Miyai T., Fujishiro H., Kawamura M., Yasuda T., Hijikata A., Bin B., Irié T., Tanaka J., Atsumi T., et al. Zinc transporter SLC39A10/ZIP10 controls humoral immunity by modulating B-cell receptor signal strength. Proc. Natl. Acad. Sci. USA. 2014;111:11786-11791.

    Not in our library10.1073/pnas.1323557111

  96. 96.

    Rosenkranz E., Metz C.H., Maywald M., Hilgers R.D., Wessels I., Senff T., Haase H., Jager M., Ott M., Aspinall R., et al. Zinc supplementation induces regulatory T cells by inhibition of Sirt-1 deacetylase in mixed lymphocyte cultures. Mol. Nutr. Food Res. 2016;60:661-667.

    Not in our library10.1002/mnfr.201500524

  97. 97.

    Rosenkranz E., Maywald M., Hilgers R.D., Brieger A., Clarner T., Kipp M., Plumakers B., Meyer S., Schwerdtle T., Rink L. Induction of regulatory T cells in Th1-/Th17-driven experimental autoimmune encephalomyelitis by zinc administration. J. Nutr. Biochem. 2016;29:116-123.

    Not in our library10.1016/j.jnutbio.2015.11.010

  98. 98.

    Kitabayashi C., Fukada T., Kanamoto M., Ohashi W., Hojyo S., Atsumi T., Ueda N., Azuma I., Hirota H., Murakami M., et al. Zinc suppresses Th17 development via inhibition of STAT3 activation. Int. Immunol. 2010;22:375-386.

    Not in our library10.1093/intimm/dxq017

  99. 99.

    Bredholt M., Frederiksen J.L. Zinc in multiple sclerosis: A systematic review and meta-analysis. ASN Neuro. 2016;8.

    Not in our library10.1177/1759091416651511

  100. 100.

    Socha K., Karpinska E., Kochanowicz J., Soroczynska J., Jakoniuk M., Wilkiel M., Mariak Z.D., Borawska M.H. Dietary habits; concentration of copper, zinc, and Cu-to-Zn ratio in serum and ability status of patients with relapsing-remitting multiple sclerosis. Nutrition. 2017;39:76-81.

    Not in our library10.1016/j.nut.2017.03.009

  101. 101.
    Pathogenic implications of distinct patterns of iron and zinc in chronic MS lesions · 2017
    No notice
  102. 102.

    Campo C.A., Wellinghausen N., Faber C., Fischer A., Rink L. Zinc inhibits the mixed lymphocyte culture. Biol. Trace Elem. Res. 2001;79:15-22.

    Not in our library10.1385/bter:79:1:15

  103. 103.

    Faber C., Gabriel P., Ibs K.H., Rink L. Zinc in pharmacological doses suppresses allogeneic reaction without affecting the antigenic response. Bone Marrow Transpl. 2004;33:1241-1246.

    Not in our library10.1038/sj.bmt.1704509

  104. 104.

    Kown M.H., van der Steenhoven T.J., Jahncke C.L., Mari C., Lijkwan M.A., Koransky M.L., Blankenberg F.G., Strauss H.W., Robbins R.C. Zinc chloride-mediated reduction of apoptosis as an adjunct immunosuppressive modality in cardiac transplantation. J. Heart Lung Transplant. 2002;21:360-365.

    Not in our library10.1016/s1053-2498(01)00384-9

  105. 105.

    Schubert C., Guttek K., Grungreiff K., Thielitz A., Buhling F., Reinhold A., Brocke S., Reinhold D. Oral zinc aspartate treats experimental autoimmune encephalomyelitis. Biometals. 2014;27:1249-1262.

    Not in our library10.1007/s10534-014-9786-8

  106. 106.

    Rungby J. Zinc, zinc transporters and diabetes. Diabetologia. 2010;53:1549-1551.

    Not in our library10.1007/s00125-010-1793-x

  107. 107.

    Jansen J., Karges W., Rink L. Zinc and diabetes—Clinical links and molecular mechanisms. J. Nutr. Biochem. 2009;20:399-417.

    Not in our library10.1016/j.jnutbio.2009.01.009

  108. 108.

    Nicolson T.J., Bellomo E.A., Wijesekara N., Loder M.K., Baldwin J.M., Gyulkhandanyan A.V., Koshkin V., Tarasov A.I., Carzaniga R., Kronenberger K. Insulin storage and glucose homeostasis in mice null for the granule zinc transporter ZnT8 and studies of the type 2 diabetes–associated variants. Diabetes. 2009;58:2070-2083.

    Not in our library10.2337/db09-0551

  109. 109.

    Lemaire K., Ravier M.A., Schraenen A., Creemers J.W., Van de Plas R., Granvik M., Van Lommel L., Waelkens E., Chimienti F., Rutter G. Insulin crystallization depends on zinc transporter ZnT8 expression, but is not required for normal glucose homeostasis in mice. Proc. Natl. Acad. Sci. USA. 2009;106:14872-14877.

    Not in our library10.1073/pnas.0906587106

  110. 110.

    Wijesekara N., Dai F., Hardy A., Giglou P., Bhattacharjee A., Koshkin V., Chimienti F., Gaisano H., Rutter G., Wheeler M. Beta cell-specific ZnT8 deletion in mice causes marked defects in insulin processing, crystallisation and secretion. Diabetologia. 2010;53:1656-1668.

    Not in our library10.1007/s00125-010-1733-9

  111. 111.

    Liuzzi J.P., Lichten L.A., Rivera S., Blanchard R.K., Aydemir T.B., Knutson M.D., Ganz T., Cousins R.J. Interleukin-6 regulates the zinc transporter Zip14 in liver and contributes to the hypozincemia of the acute-phase response. Proc. Natl. Acad. Sci. USA. 2005;102:6843-6848.

    Not in our library10.1073/pnas.0502257102

  112. 112.

    Aburto-Luna V., Treviño S., Santos-López G., Moroni-González D., Calva-Cruz O., Aguilar-Alonso P., León-Chávez B.A., Brambila E. Hepatic mobilization of zinc after an experimental surgery, and its relationship with inflammatory cytokines release, and expression of metallothionein and Zip14 transporter. Inflamm. Res. 2017;66:167-175.

    Not in our library10.1007/s00011-016-1003-5

  113. 113.

    Bonaventura P., Lamboux A., Albarède F., Miossec P. A Feedback Loop between Inflammation and Zn Uptake. PLoS ONE. 2016;11:e0147146.

    Not in our library10.1371/journal.pone.0147146

  114. 114.

    Davis C.D., Uthus E.O. DNA methylation, cancer susceptibility, and nutrient interactions. Exp. Biol. Med. 2004;229:988-995.

    Not in our library10.1177/153537020422901002

  115. 115.

    Uriu-Adams J.Y., Keen C.L. Zinc and reproduction: Effects of zinc deficiency on prenatal and early postnatal development. Birth Defects Res. B Dev. Reprod. Toxicol. 2010;89:313-325.

    Not in our library10.1002/bdrb.20264

  116. 116.

    Beach R.S., Gershwin M.E., Hurley L.S. Gestational zinc deprivation in mice: Persistence of immunodeficiency for three generations. Science. 1982;218:469-471.

    Not in our library10.1126/science.7123244

  117. 117.

    Tomat A.L., Inserra F., Veiras L., Vallone M.C., Balaszczuk A.M., Costa M.A., Arranz C. Moderate zinc restriction during fetal and postnatal growth of rats: Effects on adult arterial blood pressure and kidney. Am. J. Physiol. Regul. Integr. Comp. Physiol. 2008;295:543-549.

    Not in our library10.1152/ajpregu.00050.2008

  118. 118.

    Valera P., Zavattari P., Albanese S., Cicchella D., Dinelli E., Lima A., De Vivo B. A correlation study between multiple sclerosis and type 1 diabetes incidences and geochemical data in Europe. Environ. Geochem. Health. 2014;36:79-98.

    Not in our library10.1007/s10653-013-9520-4

  119. 119.

    Valera P., Zavattari P., Sanna A., Pretti S., Marcello A., Mannu C., Targhetta C., Bruno G., Songini M. Zinc and Other Metals Deficiencies and Risk of Type 1 Diabetes: An Ecological Study in the High Risk Sardinia Island. PLoS ONE. 2015;10:e0141262.

    Not in our library10.1371/journal.pone.0141262

  120. 120.

    Dinelli E., Lima A., De Vivo B., Albanese S., Cicchella D., Valera P. Hydrogeochemical analysis on Italian bottled mineral waters: Effects of geology. J. Geochem. Explor. 2010;107:317-335.

    Not in our library10.1016/j.gexplo.2010.06.004

  121. 121.

    Cicchella D., Albanese S., De Vivo B., Dinelli E., Giaccio L., Lima A., Valera P. Trace elements and ions in Italian bottled mineral waters: Identification of anomalous values and human health related effects. J. Geochem. Explor. 2010;107:336-349.

    Not in our library10.1016/j.gexplo.2010.04.004

  122. 122.

    Dinelli E., Lima A., Albanese S., Birke M., Cicchella D., Giaccio L., Valera P., De Vivo B. Comparative study between bottled mineral and tap water in Italy. J. Geochem. Explor. 2012;112:368-389.

    Not in our library10.1016/j.gexplo.2011.11.002

  123. 123.

    Dinelli E., Lima A., Albanese S., Birke M., Cicchella D., Giaccio L., Valera P., De Vivo B. Major and trace elements in tap water from Italy. J. Geochem. Explor. 2012;112:54-75.

    Not in our library10.1016/j.gexplo.2011.07.009

  124. 124.

    El Amari K., Valera P., Hibti M., Pretti S., Marcello A., Essarraj S. Impact of mine tailings on surrounding soils and ground water: Case of Kettara old mine, Morocco. J. Afr. Earth Sci. 2014;100:437-449.

    Not in our library10.1016/j.jafrearsci.2014.07.017

  125. 125.

    Pompili M., Vichi M., Dinelli E., Pycha R., Valera P., Albanese S., Lima A., De Vivo B., Cicchella D., Fiorillo A., et al. Relationships of local lithium concentrations in drinking water to regional suicide rates in Italy. World J. Biol. Psychiatry. 2015;16:567-574.

    Not in our library10.3109/15622975.2015.1062551

  126. 126.

    Pompili M., Vichi M., Dinelli E., Erbuto D., Pycha R., Serafini G., Giordano G., Valera P., Albanese S., Lima A., et al. Arsenic: Association of regional concentrations in drinking water with suicide and natural causes of death in Italy. Psychiatry Res. 2017;249:311-317.

    Not in our library10.1016/j.psychres.2017.01.041

  127. 127.

    Scheib A.J., Flight D.M.A., Birke M., Tarvainen T., Locutura J., Albanese S., Andersson M., Arnoldussen A., Baritz R., Batista M.J., et al. The geochemistry of niobium and its distribution and relative mobility in agricultural soils of Europe. Geochem. Explor. Environ. A. 2012;12:293-302.

    Not in our library10.1144/geochem2011-096

  128. 128.

    Mann A., Reimann C., De Caritat P., Turner N., Birke M., Albanese S., Andersson M., Baritz R., Batista M.J., Bel-Lan A., et al. Mobile metal ion® analysis of european agricultural soils: Bioavailability, weathering, Geogenic patterns and anthropogenic anomalies. Geochem. Explor. Environ. A. 2015;15:99-112.

    Not in our library10.1144/geochem2014-279

  129. 129.

    Négrel P., Sadeghi M., Ladenberger A., Reimann C., Birke M., Albanese S., Andersson M., Baritz R., Batista M.J., Bel-Lan A., et al. Geochemical fingerprinting and source discrimination of agricultural soils at continental scale. Chem. Geol. 2015;396:1-15.

    Not in our library10.1016/j.chemgeo.2014.12.004

  130. 130.

    Ladenberger A., Demetriades A., Reimann C., Birke M., Sadeghi M., Uhlbäck J., Andersson M., Jonsson E., Albanese S., Baritz R., et al. GEMAS: Indium in agricultural and grazing land soil of Europe—Its source and geochemical distribution patterns. J. Geochem. Explor. 2015;154:61-80.

    Not in our library10.1016/j.gexplo.2014.11.020

  131. 131.

    Birke M., Reimann C., Oorts K., Rauch U., Demetriades A., Dinelli E., Ladenberger A., Halamić J., Gosar M., Jähne-Klingberg F. The GEMAS Project Team. Use of GEMAS data for risk assessment of cadmium in European agricultural and grazing land soil under the REACH Regulation. Appl. Geochem. 2016;74:109-121.

    Not in our library10.1016/j.apgeochem.2016.08.014

  132. 132.

    Birke M., Reimann C., Rauch U., Ladenberger A., Demetriades A., Jähne-Klingberg F., Oorts K., Gosar M., Dinelli E., Halamić J. GEMAS: Cadmium distribution and its sources in agricultural and grazing land soil of Europe—Original data versus clr-transformed data. J. Geochem. Explor. 2017;173:13-30.

    Not in our library10.1016/j.gexplo.2016.11.007

  133. 133.

    Scheib A.J., Birke M., Dinelli E., Albanese S., Andersson M., Baritz R., Batista M.J., Bel-Lan A., Cicchella D., Demetriades A., et al. Geochemical evidence of aeolian deposits in European soils. Boreas. 2014;43:175-192.

    Not in our library10.1111/bor.12029

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