Dissecting the role of CD4+ T cells in autoimmune diabetes through the use of TCR transgenic mice.
Insulin-dependent diabetes mellitus (IDDM) is an immunological disorder wherein autoimmune-mediated destruction of islet cells in the pancreas results in persistent hyperglycemia. The non-obese diabetic mouse model of IDDM has revealed the importance of multiple factors that impact upon the disease process; however, understanding of primary immune mechanisms leading to IDDM remains elusive. The emergence of transgenic mouse models for IDDM has made important contributions towards clarifying many of these factors, including the cell types, the various effector molecules and the genetic elements involved in the pathogenesis of IDDM. In this review, we will focus on the primary mechanism and mediators of islet beta-cell death, the impact of T-helper lymphocytes on disease progression and the potential role of major histocompatibility complex class II molecules in conferring susceptibility to IDDM.
Suri
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Department of Pathology, Center for Immunology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Katz
J D
JD
D000818:Animals; D017209:Apoptosis; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D003922:Diabetes Mellitus, Type 1 / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D005802:Genes, MHC Class II; D006801:Humans; D007515:Islets of Langerhans / Q000276:immunology / Q000473:pathology; D051379:Mice; D016688:Mice, Inbred NOD; D008822:Mice, Transgenic; D011948:Receptors, Antigen, T-Cell / Q000235:genetics
D011948:Receptors, Antigen, T-Cell