期刊
JOURNAL OF INFECTIOUS DISEASES
卷 207, 期 4, 页码 638-650出版社
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jis730
关键词
PAR-1; T cells; thrombin; HIV pathogenesis; coagulation; inflammation
资金
- National Institute of Allergy and Infectious Diseases, National Institute of Health (NIH)
- National Cancer Institute, NIH [HHSN261200800001E]
Disruption of vascular integrity by trauma and other tissue insults leads to inflammation and activation of the coagulation cascade. The serine protease thrombin links these 2 processes. The proinflammatory function of thrombin is mediated by activation of protease-activated receptor 1 (PAR-1). We found that peripheral blood effector memory CD4(+) and CD8(+) T lymphocytes expressed PAR-1 and that expression was increased in CD8(+) T cells from human immunodeficiency virus (HIV)-infected patients. Thrombin enhanced cytokine secretion in CD8(+) T cells from healthy controls and HIV-infected patients. In addition, thrombin induced chemokinesis, but not chemotaxis, of CD8(+) T cells, which led to structural changes, including cell polarization and formation of a structure rich in F-actin and phosphorylated ezrin-radexin-moesin proteins. These findings suggest that thrombin mediates cross-talk between the coagulation system and the adaptive immune system at sites of vascular injury through increased T-cell motility and production of proinflammatory cytokines.
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