| Autor: |
Hurley A; CMRS/Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892-1360, USA., Smith M, Karpova T, Hasley RB, Belkina N, Shaw S, Balenga N, Druey KM, Nickel E, Packard B, Imamichi H, Hu Z, Follmann D, McNally J, Higgins J, Sneller M, Lane HC, Catalfamo M |
| Jazyk: |
angličtina |
| Zdroj: |
The Journal of infectious diseases [J Infect Dis] 2013 Feb 15; Vol. 207 (4), pp. 638-50. Date of Electronic Publication: 2012 Nov 29. |
| DOI: |
10.1093/infdis/jis730 |
| Abstrakt: |
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. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
|
