Journal
IMMUNITY
Volume 28, Issue 5, Pages 687-697Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2008.03.016
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Funding
- Howard Hughes Medical Institute Funding Source: Medline
- NCRR NIH HHS [S10 RR014884-01] Funding Source: Medline
- NIAID NIH HHS [R37 AI046643, T32 AI007090-21, R01 AI050834-06A1, R37 AI046643-10, P01 AI035297, T32 AI007090, R01 AI050834, P01 AI035297-109002] Funding Source: Medline
- NIDDK NIH HHS [P30 DK063720-01, P30 DK063720] Funding Source: Medline
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The dynamics of CD4(+) effector T cells (Teff cells) and CD4(+)Foxp3(+) regulatory T cells (Treg cells) during diabetes progression in nonobese diabetic mice was investigated to determine whether an imbalance of Treg cells and Teff cells contributes to the development of type 1 diabetes. Our results demonstrated a progressive decrease in the Treg cell:Teff cell ratio in inflamed islets but not in pancreatic lymph nodes. Intra-islet Treg cells expressed reduced amounts of CD25 and Bcl-2, suggesting that their decline was due to increased apoptosis. Additionally, administration of low-dose interleukin-2 (IL-2) promoted Treg cell survival and protected mice from developing diabetes. Together, these results suggest intra-islet Treg cell dysfunction secondary to defective IL-2 production is a root cause of the progressive breakdown of self-tolerance and the development of diabetes in nonobese diabetic mice.
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