期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 204, 期 8, 页码 1765-1774出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20070719
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资金
- NCI NIH HHS [CA123079, R01 CA123079] Funding Source: Medline
- NIAID NIH HHS [AI048667, R01 AI048667] Funding Source: Medline
We demonstrate that all-trans retinoic acid (RA) induces Ill adaptive T regulatory cells (A-Tregs) to acquire a gut-homing phenotype (alpha 4 beta 7(+) CC chemokine receptor 9(+)) and the capacity to home to the lamina propria of the small intestine. Under conditions that favor the differentiation of A-Tregs (transforming growth factor-beta 1 and interleukin 2) in vitro, the inclusion of RA induces nearly all activated Cl T cells to express FoxP3 and greatly increases the accumulation of these cells. In the absence of RA, A-Treg differentiation is abruptly impaired by proficient antigen presenting cells or through direct co-stimulation. In the presence of RA, A-Treg generation occurs even in the presence of high levels of co-stimulation, with RA attenuating co-stimulation from interfering from Ill induction. The recognition that RA induces gut imprinting, together with our finding that it enhances A-Treg conversion, differentiation, and expansion, indicates that RA production in vivo may drive both the imprinting and A-Treg development in the face of overt inflammation.
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