Primate Monocytes - CD14, CD16 - Ziegler-Heitbrock

Characterization of Immune Failure by Monocyte Activation Phenotypes in HIV-Infected Patients Receiving Antiretroviral Therapy.

Abstract

TO THE EDITOR—Wilson et al [1] demonstrated that, in human immunodeficiency virus (HIV)–infected subjects, levels of inflammatory biomarkers known to be associated with increased clinical risk (interleukin 6, D-dimer, high sensitive reactive-C protein, soluble CD14, and soluble CD163) are more closely related to markers of monocyte activation and migration than to markers of T-cell activation. These data suggest that monocytes may play a prominent role in chronic and serious non-AIDS events, such as premature cardiovascular disease and cancer. Meanwhile, several large cohort studies have demonstrated that HIVinfected subjects who do not undergo full CD4+ T-cell restoration during antiretroviral therapy (ART) (ie, those with immune failure [IF]) are at greater risk of developing these non-AIDS conditions [2–6]. Based on the findings of Wilson et al [1], we investigated monocyte activation phenotypes