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The non-obese diabetic (NOD) mouse is considered to be a good model of human Type I diabetes mellitus. Both sexes develop insulitis starting at about 6 weeks of age, and onset of diabetes follows at about 30 weeks in females, but later and much less frequently in males. In some mice (but not all) infiltration of the islets leads to selective destruction of insulin-producing beta cells, which is marked by clinically overt diabetes and is thought to be an autoimmune response mediated by T cells. Both L3T4+ and Ly2+ cells have been implicated in the destructive process and we have used an in vivo transfer system, together with histological studies on the pancreas, to demonstrate the essential role played by Ly2+ T cells in the destruction of beta cells in diabetic mice.

Original publication

DOI

10.1016/s0896-8411(09)90018-x

Type

Journal article

Journal

Journal of autoimmunity

Publication Date

04/1990

Volume

3 Suppl 1

Pages

101 - 109

Addresses

Department of Immunology, University College and Middlesex School of Medicine, London, UK.

Keywords

Islets of Langerhans, Spleen, T-Lymphocytes, Animals, Mice, Mice, Mutant Strains, Diabetes Mellitus, Experimental, Antigens, Ly, Immunization, Passive, Female, Male