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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.
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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,

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The Journal of infectious diseases 2016 10 04214(12) 1808-1816

Abstract

Increases in inflammation, coagulation, and CD8(+) T-cell numbers are associated with an elevated cardiovascular disease (CVD) risk in human immunodeficiency virus (HIV)-infected antiretroviral therapy (ART) recipients. Circulating memory CD8(+) T cells that express the vascular endothelium-homing receptor CX3CR1 (fractalkine receptor) are enriched in HIV-infected ART recipients. Thrombin-activated receptor (PAR-1) expression is increased in HIV-infected ART recipients 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 interferon γ production by purified CD8(+) T cells but was attenuated by thrombin-induced release of transforming growth factor 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 HIV-infected ART recipients.

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