Protective role of infections and vaccinations on autoimmune diseases

Abstract

Infectious agents may induce autoimmune disease through several mechanisms, notably antigen mimicry and inflammation of the target organ; conversely, infections may protect from autoimmune diseases. This paradoxical effect has been demonstrated for a number of bacteria, viruses and parasites on a variety of spontaneous or experimentally induced animal models of autoimmune diseases (e.g. experimental allergic encephalomyelitis, lupus mice, non-obese diabetic mice). The mechanisms of the protection are still ill-defined, and probably vary according to models. Stimulation of immunoregulatory CD4 T cells has been shown to play a central role in several major models. The role of superantigens is also important, like that of Toll-like receptors. Antigen competition is another major mechanism, itself open to several interpretations. Epidemiological data support a protective role of infections on human allergic and autoimmune diseases. These diseases are much more common in countries with high socio-economic development (typically Northern countries in Europe). The reason for this cannot be fully explained by genetic differences because migrating populations develop these diseases with the same incidence of the adoptive country rather than that of the country of origin. It is interesting that the frequency of these diseases has been increasing in developed countries over the last 20 years but not in undeveloped ones.