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The FASEB Journal, Vol 7, 1092-1096, Copyright © 1993 by The Federation of American Societies for Experimental Biology

REVIEWS

Autoimmune diabetes results from genetic defects manifest by antigen presenting cells

DV Serreze
Jackson Laboratory, Bar Harbor, Maine 04609.

In most cases, insulin-dependent diabetes results from autoimmune elimination of pancreatic beta cells by T lymphocytes that are generated as a result of complex polygenic interactions between particular MHC haplotypes and non-MHC linked susceptibility modifiers. Immature T cells with potential autoreactivity are normally destroyed in the thymus when they are highly activated after ligation of the T cell receptor (TCR) with "self" peptides bound to MHC molecules on antigen presenting cells (APC) such as macrophages. Here the hypothesis is put forth that non-MHC linked diabetes susceptibility genes contribute to subtle defects in the maturation of macrophages, and in synergy with a diabetogenic MHC haplotype generate APC that are unable to trigger autoreactive T cells to an activation state high enough to induce their destruction.


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Copyright © 1993 by The Federation of American Societies for Experimental Biology.