Failure in immune regulation begets IDDM in NOD mice.
The nonobese diabetic (NOD) mouse model of insulin-dependent diabetes mellitus (IDDM) has provided evidence which suggests that an important mechanism of the induction of this T-cell-mediated autoimmune disease is a failure in immune regulation. The role of T-cell immune dysregulation in the initiation of diabetes is the focus of this review. Immunological mechanisms such as T-cell anergy and deficient T-cell-mediated suppression are discussed as mediators of IDDM susceptibility. In particular, T helper (Th) 2 cell anergy may be responsible for defective regulation of autoreactive effector T-cells. Therapies designed to overcome these T-cell-mediated deficiencies may prevent IDDM onset.
John P. Robarts Research Institute, University of Western Ontario, London, Canada.
M J
MJ
Cameron
C
C
Meagher
T L
TL
Delovitch
D000818:Animals; D001324:Autoantigens / Q000276:immunology; D003922:Diabetes Mellitus, Type 1 / Q000276:immunology*; D008285:Major Histocompatibility Complex / Q000276:immunology; D051379:Mice; D016688:Mice, Inbred NOD / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
D001324:Autoantigens