Antigen mimicry between infectious agents and self or environmental antigens may lead to long-term regulation of inflammation

The PasT Influences The PresenT: InfecTIons Induce an ImmunologIcal sTaTe ThaT conTrols The develoPmenT of allergy, aToPy, and auToImmune dIseasesTo account for the increasing prevalences of allergic and autoimmune diseases in populations that partake of good hygiene conditions, and, therefore, are less exposed to pathogens, the hygiene hypothesis proposes that infections favor the long-lasting control of types I and IV hypersensitivity reactions (1).This effect has been ascribed to interleukin (IL-)10 production (2-4).However, type I hypersensitivity can still be kept in check well after the infection has subsided (5), and past infections may protect against the development of autoimmunity (4, 6).In one study, 613 individuals from two African villages with different prevalences of schistosomiasis caused by Schistosoma haematobium were investigated for the presence of circulating anti-nuclear autoantibodies (ANA).ANA levels were lower in the most heavily infected individuals in the low schistosomiasis-prevalence village, although no statistically significant differences among differently infected groups was reported.A statistically significant, but small mean difference of about 3 IU between treated and untreated individuals was observed, a fact that allows one to conclude that ongoing Antigen mimicry between infectious agents and self or environmental antigens may lead to long-term regulation of inflammation

Abstract licence: CC BY

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