期刊
JOURNAL OF IMMUNOLOGY
卷 174, 期 12, 页码 7487-7491出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.174.12.7487
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资金
- NIAID NIH HHS [R01 AI 65016] Funding Source: Medline
- NIDDK NIH HHS [P01 DK46763] Funding Source: Medline
Transfer of CD4(+)CD45RB(high) T cells into RAG(-/-) mice causes colitis, which can be prevented by CD4(+) CD25(+) regulatory T cells (Treg). Colitis induction by CD4(+) CD45RB(high) T cells requires beta(7) integrin-dependant intestinal localization, hut the importance beta(7) integrins for Treg function is unknown. In this study, we show that beta(-/-)(7) Treg were effective in preventing colitis. Treg expanded in vivo to the same extent as CD4(+) CD45RB(high) T cells after transfer and they did not inhibit CD4(+) CD45RB(high) T cell expansion in lymphoid tissues, although they prevented the accumulation of Th1 effector cells in the intestine. beta(-/-)(7) Treg were significantly reduced in the large intestine, however, compared with wild-type Treg, and regulatory activity could not he recovered from the intestine of recipients of beta(-/-)(7) Treg. These data demonstrate that Treg can prevent colitis by inhibiting the accumulation of tissue-seeking effector cells and that Treg accumulation in the intestine is dispensable for colitis suppression.
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