description
Type I diabetes mellitus is a disease that results from autoimmune destruction of the insulin-producing beta-cells. Certain beta-cell proteins act as autoantigens after being processed by antigen-presenting cell (APC), such as macrophages and dendritic cells, and presented in a complex with MHC-II molecules on the surface of the APC. Then immunogenic signals from APC activate CD4+ T cells, predominantly of the Th1 subset. Antigen-activated Th1 cells produce IL-2 and IFNgamma. They activate macrophages and cytotoxic CD8+ T cells, and these effector cells may kill islet beta-cells by one or both of two types of mechanisms: (1) direct interactions of antigen-specific cytotoxic T cells with a beta-cell autoantigen-MHC-I complex on the beta-cell, and (2) non-specific inflammatory mediators, such as free radicals/oxidants and cytokines (IL-1, TNFalpha, TNFbeta, IFNgamma). Type I diabetes is a polygenic disease. One of the principle determining genetic factors in diabetes incidence is the inheritance of mutant MHC-II alleles. Another plausible candidate gene is the insulin gene

external resources
NCBI:83095
KEGG:hsa04940
PUBMED:11507694
PUBMED:8072542
PUBMED:15889095
PUBMED:15889096
PUBMED:12796471
PUBMED:14617043
PUBMED:8786033
PUBMED:9719467
PUBMED:12752668

genes
FAS , FASLG , CD28 , CD80 , CD86 , CPE , GAD1 , GAD2 , GZMB , HLA-A , HLA-B , HLA-C , HLA-DMA , HLA-DMB , HLA-DOA , HLA-DOB , HLA-DPA1 , HLA-DPB1 , HLA-DQA1 , HLA-DQA2 , HLA-DQB1 , HLA-DRA , HLA-DRB1 , HLA-DRB5 , HLA-E , HLA-F , HLA-G , HSPD1 , ICA1 , IFNG , IL1A , IL1B , IL2 , IL12A , IL12B , INS , LTA , PRF1 , PTPRN , PTPRN2 , TNF ,