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Autoimmune diabetes results from genetic defects manifest by antigen presenting cells
Author(s) -
Serreze David V.
Publication year - 1993
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.7.11.8370480
Subject(s) - major histocompatibility complex , t cell receptor , immunology , biology , antigen , t cell , autoimmunity , microbiology and biotechnology , immune system
In most cases, insulin‐dependent diabetes results from autoimmune elimination of pancreatic β 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.—Serreze, D. V. Autoimmune diabetes results from genetic defects manifest by antigen presenting cells. FASEB J. 7: 1092‐1096; 1993.