Abstract
Type 1 Diabetes (T1D) is an autoimmune disease that results from the selective destruction of insulin‐producing beta cells in the pancreas. While it is generally believed that viral infections are responsible for inducing autoimmunity in individuals at risk, experimental evidence indicates that viruses can efficiently prevent T1D. We have identified two mechanisms by which acute lymphocytic choriomeningitis virus (LCMV) infection hampers autoimmune diabetes development in the mouse.The first mechanism is the direct consequence of the early release of inflammatory mediators following LCMV challenge which rapidly confer leukocytes from infected mice the capacity to diminish T1D. The second mechanism involves longer‐term modification of CD4+CD25+ regulatory T cells which become capable of preventing both spontaneous and virally induced T1D as a consequence of TGF‐beta production. Importantly, hampering of autoimmunity by viral infection does not appear to impair antiviral immunity and viral clearance.These findings provide novel mechanistic insight into the ability of viral infection to abort autoimmune diabetes. Induction of such mechanisms during infection may account for the capacity of viruses to prevent T1D as well as other autoimmune disorders.
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