Primate Monocytes - CD14, CD16 - Ziegler-Heitbrock

Shared monocyte subset phenotypes in HIV-1 infection and in uninfected subjects with acute coronary syndromes

Abstract

The mechanisms responsible for increased cardiovascular risk associated with HIV-1 infection are incompletely defined. Using flow cytometry, we examined activation phenotypes of monocyte subpopulations in patients with HIV-1 infection or acute coronary syndromes (ACS) to find common cellular profiles. Non-classical (CD14(+)CD16(++)) and Intermediate (CD14(++)CD16(+)) monocytes are proportionally increased and express high levels of tissue factor (TF) and CD62P in HIV-1 infection. These proportions are related to viremia, to T cell activation, and to plasma levels of IL-6. In vitro exposure of whole blood samples from uninfected control donors to LPS increased surface TF expression on all monocyte subsets, but, exposure to HIV-1 resulted in activation only of non-classical monocytes. Remarkably, the profile of monocyte activation in uncontrolled HIV-1 disease mirrors that of acute coronary syndromes (ACS) in uninfected persons. Thus, drivers of immune activation and inflammation in HIV-1 disease may alter monocyte subpopulations and activation phenotype, contributing to a pro-atherothrombotic state that may drive cardiovascular risk in HIV-1 infection.