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(Journal Article): Tumor necrosis factor-alpha regulation of CD4+CD25+ T cell levels in NOD mice.
Wu AJ, Hua H, Munson SH, McDevitt HO (Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.)
IN:
Proc Natl Acad Sci U S A
2002; 99(19):12287-12292
Impact Factor(s) of Proc Natl Acad Sci U S A: 10.452 (2004), 10.272 (2003), 10.7 (2002), 10.896 (2001)
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ABSTRACT: The mechanism by which tumor necrosis factor-alpha (TNF) differentially modulates type I diabetes mellitus in the nonobese diabetic (NOD) mouse is not well understood. CD4+CD25+ T cells have been implicated as mediators of self-tolerance. We show (i) NOD mice have a relative deficiency of CD4+CD25+ T cells in thymus and spleen; (ii) administration of TNF or anti-TNF to NOD mice can modulate levels of this population consistent with their observed differential age-dependent effects on diabetes in the NOD mouse; (iii) CD4+CD25+ T cells from NOD mice treated neonatally with TNF show compromised effector function in a transfer system, whereas those treated neonatally with anti-TNF show no alteration in ability to prevent diabetes; and (iv) repeated injection of CD4+CD25+ T cells into neonatal NOD mice delays diabetes onset for as long as supplementation occurred. These data suggest that alterations in the number and function of CD4+CD25+ T cells may be one mechanism by which TNF and anti-TNF modulate type I diabetes mellitus in NOD mice.
TYPE OF PUBLICATION: Original article
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