期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 99, 期 19, 页码 12287-12292出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.172382999
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资金
- NIDCR NIH HHS [F32 DE05713-03, F32 DE005713] Funding Source: Medline
- NIDDK NIH HHS [R01 DK051705, DK51705] Funding Source: Medline
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; (it) 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.
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