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 ha
s been demonstrated for a number of bacteria, viruses and parasites on a va
riety of spontaneous or experimentally induced animal models of autoimmune
diseases (e.g. experimental allergic encephalomyelitis, lupus mice, non-obe
se 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 inte
rpretations. Epidemiological data support a protective role of infections o
n human allergic and autoimmune diseases. These diseases are much more comm
on in countries with high socio-economic development (typically Northern co
untries in Europe). The reason for this cannot be fully explained by geneti
c 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 inc
reasing in developed countries over the last 20 years but not in undevelope
d ones. (C) 2001 Academic Press.