COCAINE BLUNTS HUMAN CD4(+) CELL ACTIVATION

Cocaine is reported to be immunotoxic. The biochemical mechanisms resp onsible for the immunopharmacological outcomes of cocaine in vivo and in vitro remain, however, to be fully elucidated. Our experimental dat a confirm that exposure of normal human T cells to micromolar concentr ations of cocaine modulates T-cell responses to stimulation by a varie ty of stimuli, and indicate that cocaine impairs early activation even ts during CD4(+) but not CD4(-) T-cell stimulation. Pre-incubation of enriched CD4(+) T-cell subpopulations that express the homing receptor CD62L with nanomolar concentrations of the endogenous opioid peptide beta-endorphin leads to a more severe impairment of activation than th at noted following pre-incubation with micromolar concentrations of co caine alone. These findings begin to elucidate the molecular and cellu lar mechanisms of the immunopathology of cocaine. Our data support the proposition that cocaine abuse may place cocaine-abuser HIV-seroposit ive individuals at increased risk of opportunistic infections.