Defective monocyte function in acquired immune deficiency syndrome (AIDS): evidence from a monocyte-dependent T-cell proliferative system

Abstract

T-cell proliferative responses to the mitogenic monoclonal antibody anti-Leu 4 were assessed in healthy controls, lymphadenopathy syndrome (LAS) patients, and acquired immune deficiency syndrome (AIDS) patients. While 19% of the control group showed low anti-Leu 4 responses (less than 12,000 cpm), 60% of the LAS patients, 71% of the AIDS-opportunistic infection patients, and 50% of the AIDS-Kaposi's sarcoma patients showed low responses. T-cell responsiveness in healthy low responders was greatly enhanced by the addition of monocytes from an anti-Leu 4 high responder (responder monocytes). We therefore sought to determine if the low-responder state in LAS and AIDS patients was also mediated by monocytes and, thus, correctable by the addition of responder monocytes. In the LAS low-responder group, the level of enhancement by healthy responder monocytes was similar to that observed for the healthy low-responder group. In the AIDS low-responder group, however, the level of enhancement was significantly lower than that observed in the healthy low-responder and LAS low-responder groups. These findings suggest that impaired proliferation to anti-Leu 4 in LAS patients may be due to a monocyte defect similar to the monocyte defect responsible for low anti-Leu 4 responses in healthy controls. AIDS patients, however, show additional defects in anti-Leu 4-induced proliferation that are not fully corrected by the addition of responder monocytes.