An Interleukin (IL)-10/IL-12 Immunoregulatory Circuit Controls Susceptibility to Autoimmune Disease

doi:10.1084/jem.187.4.537

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J. Exp. Med., Volume 187, Number 4, February 16, 1998 537-546

An Interleukin (IL)-10/IL-12 Immunoregulatory Circuit Controls Susceptibility to Autoimmune Disease

By Benjamin M. Segal, Bonnie K. Dwyer, and Ethan M. Shevach

From the Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892

Cells of the innate immune system secrete cytokines early in immune responses that guide maturing T helper (Th) cells alongappropriate lineages. This study investigates the role of cytokinenetworks, bridging the innate and acquired immune systems, inthe pathogenesis of an organ specific autoimmune disease. Experimentalallergic encephalomyelitis (EAE), a demyelinating disease of thecentral nervous system, is widely used as an animal model formultiple sclerosis. We demonstrate that interleukin (IL)-12 isessential for the generation of the autoreactive Th1 cells thatinduce EAE, both in the presence and absence of interferon $gamma$ .The disease-promoting effects of IL-12 are antagonized by IL-10produced by an antigen nonspecific CD4⁺ T cell which, in turn, is regulated by the endogenous productionof IL-12. This unique immunoregulatory circuit appears to playa critical role in controlling Th cell differentiation and providesa mechanism by which microbial triggers of the innate immune systemcan modulate autoimmune disease.

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