期刊
IMMUNITY
卷 16, 期 1, 页码 23-35出版社
CELL PRESS
DOI: 10.1016/S1074-7613(01)00259-X
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资金
- NCI NIH HHS [CA40041] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R01CA040041, R37CA040041] Funding Source: NIH RePORTER
CD28 and CTLA-4 engagement with B7 expressed by APCs generates critical regulatory signals for T cell activation. CD28 is expressed on the T cell surface and enhances T cell expansion, while CTLA-4 localizes primarily to an intracellular compartment and inhibits T cell proliferation. We demonstrate that CTLA-4 has several unique trafficking properties that may regulate its ability to attenuate a T cell response. Importantly, accumulation of CTLA-4 at the immunological synapse is proportional to the strength of the TCR signal, suggesting that cells receiving stronger stimuli are more susceptible to CTLA-4-mediated inhibition. This may represent a novel feedback control mechanism in which a stimulatory signal regulates the recruitment of an inhibitory receptor to a functionally relevant site on the cell surface.
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