期刊
NATURE IMMUNOLOGY
卷 6, 期 1, 页码 90-98出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni1144
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- NATIONAL CANCER INSTITUTE [P01CA069381] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [P01AI031238, R37AI033068, R01AI048073, R01AI033068] Funding Source: NIH RePORTER
- NCI NIH HHS [CA69381] Funding Source: Medline
- NHLBI NIH HHS [P50 HL54619] Funding Source: Medline
- NIAID NIH HHS [AI33068, AI48073, P01 AI31238] Funding Source: Medline
- NIA NIH HHS [AG00252] Funding Source: Medline
B and T lymphocyte attenuator (BTLA) provides an inhibitory signal to B and T cells. Previously, indirect observations suggested that B7x was a ligand for BTLA. Here we show that BTLA does not bind B7x; instead, we identify herpesvirus entry mediator (HVEM) as the unique BTLA ligand. BTLA bound the most membrane-distal cysteine-rich domain of HVEM, distinct from regions where the ligands LIGHT and lymphotoxin-alpha bound HVEM. HVEM induced BTLA tyrosine phosphorylation and association of the tyrosine phosphatase SHP-2 and repressed antigen-driven T cell proliferation, providing an example of reverse signaling to a non-tumor necrosis factor family ligand. The conservation of the BTLA-HVEM interaction between mouse and human suggests that this system is an important pathway regulating lymphocyte activation and/or homeostasis in the immune response.
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