Association between alphabetaTCR+CD4-CD8- T-cell deficiency and IDDM in NOD/Lt mice.

Important note: Information in this article was accurate in 1997. The state of the art may have changed since the publication date.

Association between alphabetaTCR+CD4-CD8- T-cell deficiency and IDDM in NOD/Lt mice.

Diabetes. 1997 Apr;46(4):572-82. Unique Identifier : AIDSLINE MED/97230218
Baxter AG; Kinder SJ; Hammond KJ; Scollay R; Godfrey DI; Centenary Institute of Cancer Medicine and Cell Biology, Camperdown,; Australia. a.baxter@centenary.usyd.edu.au

Abstract: NOD mice develop spontaneous IDDM as a result of T-cell-mediated autoimmune destruction of pancreatic beta-cells. It is not known why these T-cells become autoreactive, nor is it clear whether the breakdown in self-tolerance reflects a general problem in T-cell development or a selective defect in an as yet undefined regulatory cell population. In this study, we showed that NOD mice, although relatively normal with regard to most thymocyte subsets, exhibit a marked deficiency in alphabetaTCR+CD4-CD8- alphabeta+DN) T-cells in the thymus and, to a lesser extent, in the periphery. These T-cells have been termed NKT cells NK1.1+-like T-cells) because they share some cell surface markers with conventional natural killer (NK) cells. To examine the role of these cells in the pathogenesis of IDDM, semiallogeneic or syngeneic double-negative (DN) thymocytes, enriched for NKT cells, were transferred into intact 4-week-old NOD recipients; the onset of diabetes was then monitored over the ensuing 30 weeks. Mice receiving NKT-enriched thymocytes did not develop diabetes, whereas mice receiving unfractionated thymocytes or phosphate-buffered saline developed diabetes at the normal rate. NKT cells represent a distinct T-cell lineage that has been shown to play a role in immunoregulation in vivo. The deficiency of these cells observed in NOD mice may therefore contribute to destruction of pancreatic islet cells by conventional T-cells.

Keywords: *Adoptive Transfer *Antigens, CD4/ANALYSIS *Antigens, CD8/ANALYSIS *Diabetes Mellitus, Insulin-Dependent/IMMUNOLOGY *Receptors, Antigen, T-Cell, alpha-beta/ANALYSIS *T-Lymphocyte Subsets/IMMUNOLOGY *Thymus Gland/CHEMISTRY
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