Faculty Research 1990 - 1999

Autoimmune diabetes results from genetic defects manifest by antigen presenting cells.

Document Type

Article

Publication Date

1993

Keywords

Antigen-Presenting-Cells: ph, Autoimmune-Diseases: et, ge, Diabetes-Mellitus-Insulin-Dependent: et, ge, H-2-Antigens: ge, Haplotypes, Human, Islets-of-Langerhans: im, Mice, Mice-Inbred-NOD, T-Lymphocytes: im

First Page

1092

Last Page

1096

JAX Source

FASEB J 1993 Aug;7(11):1092-6

Abstract

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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