Advertisement

 

 

Inflammatory function of CX3CR1+ CD8 T cells in treated HIV infection is modulated by platelet interactions.

Inflammatory function of CX3CR1+ CD8 T cells in treated HIV infection is modulated by platelet interactions.
Author Information (click to view)

Mudd JC, Panigrahi S, Kyi B, Moon SH, Manion MM, Younes SA, Sieg SF, Funderburg NT, Zidar DA, Lederman MM, Freeman ML,


Mudd JC, Panigrahi S, Kyi B, Moon SH, Manion MM, Younes SA, Sieg SF, Funderburg NT, Zidar DA, Lederman MM, Freeman ML, (click to view)

Mudd JC, Panigrahi S, Kyi B, Moon SH, Manion MM, Younes SA, Sieg SF, Funderburg NT, Zidar DA, Lederman MM, Freeman ML,

Advertisement
Share on FacebookTweet about this on TwitterShare on LinkedIn

The Journal of infectious diseases 2016 Oct 4() pii

Abstract

Increases in inflammation, coagulation, and CD8 T cell numbers are associated with elevated cardiovascular disease (CVD) risk in antiretroviral therapy (ART)-treated HIV infection. Circulating memory CD8 T cells that express the vascular endothelium-homing receptor CX3CR1 (fractalkine receptor) are enriched in ART-treated HIV-infected subjects. Thrombin-activated receptor (PAR-1) expression is increased in ART-treated HIV-infected subjects and is particularly elevated on CX3CR1+ CD8 T cells, suggesting that these cells could interact with coagulation elements. Indeed, thrombin directly enhanced T cell receptor mediated IFNγ production by purified CD8 T cells, but was attenuated by thrombin-induced release of TGF-β by platelets. We have therefore identified a population of circulating memory CD8 T cells in HIV infection that may home to endothelium, can be activated by clot-forming elements, and are susceptible to platelet-mediated regulation. Complex interactions between inflammatory elements and coagulation at endothelial surfaces may play an important role in CVD risk in ART-treated HIV-infected individuals.

Submit a Comment

Your email address will not be published. Required fields are marked *

seventeen − 14 =

[ HIDE/SHOW ]