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Anti-CD43 monoclonal antibody L11 blocks migration of T cells to inflamed pancreatic islets and prevents development of diabetes in nonobese diabetic mice

Journal of Immunology, ISSN: 0022-1767, Vol: 163, Issue: 10, Page: 5678-5685
1999
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Article Description

Nonobese diabetic mice are a well-known model for human insulin- dependent diabetes mellitus. These mice develop autoimmune-mediated inflammation of the pancreatic islets, followed by destruction of the insulin-producing β cells and development of diabetes. Nonobese diabetic mice also have salivary gland inflammation, and serve as a model for human Sjogren's syndrome. T cells are a prominent component of the inflammatory infiltrate in these sites, and T cell recruitment from the blood is thought to be essential for the initiation and maintenance of pathologic tissue damage. A unique mAb to murine CD43, L11, has recently been shown to block the migration of T cells from blood into organized lymphoid tissues. Here we demonstrate that L11 significantly inhibits T cell migration from blood into inflamed islets and salivary glands. Treatment of nonobese diabetic mice with L11 from 1 to 4 or 8 to 12 wk of age led to significant protection against the development of diabetes. Moreover, protection was long-lived, with decreased incidence of diabetes even months after cessation of Ab administration. When treatment was started at 1 wk of age, L11 inhibited the development of inflammation in pancreatic islets and salivary glands. L11 treatment had no long-term effect on numbers or phenotypes of peripheral lymphocytes. These data indicate that anti-CD43 Abs that block T cell migration may be useful agents for the prevention or treatment of autoimmune diseases including insulin-dependent diabetes mellitus and Sjogren's syndrome.

Bibliographic Details

Gregory G. Johnson; Anna Mikulowska; Eugene C. Butcher; Sara A. Michie; Leslie M. McEvoy

Oxford University Press (OUP)

Medicine; Immunology and Microbiology

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