期刊
NATURE COMMUNICATIONS
卷 5, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms4436
关键词
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资金
- British Heart Foundation [PG 09/002/2642]
- King's College London British Heart Foundation Centre of Excellence
- Department of Health via National Institute for Health Research (NIHR) comprehensive Biomedical Research Centre
- British Heart Foundation studentship [FS/10/009/28166]
- Arthritis Research UK Fellowship [18103]
- British Heart Foundation [FS/10/009/28166, RG/09/002/26425] Funding Source: researchfish
- Cancer Research UK [15961] Funding Source: researchfish
- Versus Arthritis [18103] Funding Source: researchfish
Localization of CD4(+)CD25(+)Foxp3(+) regulatory T (Treg) cells to lymphoid and non-lymphoid tissue is instrumental for the effective control of immune responses. Compared with conventional T cells, Treg cells constitute a minute fraction of the T-cell repertoire. Despite this numeric disadvantage, Tregs efficiently migrate to sites of immune responses reaching an optimal number for the regulation of T effector (Teff) cells. The array and levels of adhesion and chemokine receptor expression by Tregs do not explain their powerful migratory capacity. Here we show that recognition of self-antigens expressed by endothelial cells in target tissue is instrumental for efficient Treg recruitment in vivo. This event relies upon IFN-gamma-mediated induction of MHC-class-II molecule expression by the endothelium and requires optimal PI3K p110 delta activation by the T-cell receptor. We also show that, once in the tissue, Tregs inhibit Teff recruitment, further enabling a Teff: Treg ratio optimal for regulation.
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