Department of Gastroenterology, Hepatology and Endocrinology, Medizinische
Hochschule Hannover, Carl-Neuberg-Str. 1, D-30623, Hannover, Germany.
Although viruses are commonly cited as triggers for autoimmune disease, the
actual mechanisms by which they initiate autoimmunity are unknown. Molecular
mimicry is the most popular hypothesis, and it proposes that viral antigens that
share homologies with host antigens generate an immune response that damages
host tissue. The viral antigen may not be needed for perpetuation of the
disease, and cross-reacting immune responses can involve humoral, cellular, or
both types of reactivity. Linear and conformational epitopes may be involved,
and foreign antigens do not need to share exact amino acid sequences with
self-proteins to activate autoreactive T cells. Bystander effects can enhance
the autoimmune process if previously sequestered or cryptic antigens are exposed
to the immune system, and superantigens that are produced by the pathogen and
are not MHC restricted can result in marked polyclonal activation of CD4 and CD8
T cells. Future studies must differentiate the targets of pathologic immunity
and distinguish self-antigens from infectious nonself-antigens. Transgenic
animal models of AIH are needed to assess the pathogenicity of the antigenic
targets.
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