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Defective activation of T suppressor cell function in nonobese diabetic mice. Potential relation to cytokine deficiencies.

D V Serreze and E H Leiter
J Immunol June 1, 1988, 140 (11) 3801-3807;
D V Serreze
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E H Leiter
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Abstract

Nonobese diabetic (NOD) is an inbred mouse strain susceptible to development of T cell-mediated autoimmune diabetes. The strain is characterized by high percentages of T lymphocytes in lymphoid organs. The syngeneic mixed lymphocyte reaction (SMLR), a T cell response to self MHC class II Ag, is reportedly involved in the generation of a number of immunoregulatory cells, including suppressor inducers. A severely depressed SMLR characteristic of certain other autoimmune strains was found in NOD but not in nonautoimmune SWR/Bm mice. Moreover, IL-2 produced by NOD T cells at day 6 in an SMLR was at least one hundredfold reduced compared with SWR, and NOD T cells harvested from an SMLR at day 6 were functionally defective when tested for ability to induce suppression of an allogeneic MLR. However, functionally competent suppressor T cells were generated in NOD splenic leukocyte cultures in response to Con A, and IL-2 release from these was equivalent to that released by Con A-stimulated SWR splenocytes. A deficiency in cytokine release was not limited to IL-2, because peritoneal exudate cells from NOD exhibited a greatly diminished sensitivity to LPS-stimulated IL-1 release in comparison to SWR mice. IL-2 supplementation both in vitro and in vivo restored the ability of NOD T cells to respond in a SMLR, with production of cells capable of inducing suppression. Like SMLR-activated T cells from untreated SWR controls, SMLR blasts from IL-2-treated NOD mice were enriched for the L3T4 phenotype. IL-1 supplementation in vitro resulted in partial restoration of T suppressor activation in a SMLR. The depressed SMLR exhibited by NOD mice was apparently a stimulator cell dysfunction, because NOD stimulator cells failed to activate T cells from (SWR x NOD)F1 mice, whereas stimulators from SWR or F1 mice were capable of doing so. Collectively, these results suggest a defect in suppressor cell activation rather than an absence of this immunoregulatory cell population.

  • Copyright © 1988 by American Association of Immunologists

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The Journal of Immunology
Vol. 140, Issue 11
1 Jun 1988
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Defective activation of T suppressor cell function in nonobese diabetic mice. Potential relation to cytokine deficiencies.
D V Serreze, E H Leiter
The Journal of Immunology June 1, 1988, 140 (11) 3801-3807;

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Defective activation of T suppressor cell function in nonobese diabetic mice. Potential relation to cytokine deficiencies.
D V Serreze, E H Leiter
The Journal of Immunology June 1, 1988, 140 (11) 3801-3807;
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Print ISSN 0022-1767        Online ISSN 1550-6606