期刊
IMMUNITY
卷 20, 期 1, 页码 37-46出版社
CELL PRESS
DOI: 10.1016/S1074-7613(03)00351-0
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资金
- NATIONAL CANCER INSTITUTE [P30CA021765, F32CA083269] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P01HL053749] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK042932] Funding Source: NIH RePORTER
- NCI NIH HHS [CA21765, 5-F32-CA83269] Funding Source: Medline
- NHLBI NIH HHS [P01 HL53749] Funding Source: Medline
- NIDDK NIH HHS [R01 DK 42932] Funding Source: Medline
T cells play a central role in the recognition and elimination of foreign pathogens. Signals through the T cell receptor (TCR) control the extent and duration of the T cell response. To ensure that T cells are not inappropriately activated, signaling pathways downstream of the TCR are subject to multiple levels of positive and negative regulation. Herein, we describe two related proteins, Sts-1 and Sts-2, that negatively regulate TCR signaling. T cells from mice lacking Sts-1 and Sts-2 are hyperresponsive to TCR stimulation. The phenotype is accompanied by increased Zap-70 phosphorylation and activation, including its ubiquitinylated forms. Additionally, hyperactivation of signaling proteins downstream of the TCR, a marked increase in cytokine production by Sts1/2(-/-) T cells, and increased susceptibility to autoimmunity in a mouse model of multiple sclerosis is observed. Therefore, Sts-1 and Sts-2 are critical regulators of the signaling pathways that regulate T cell activation.
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