Dys-regulation of effector CD4+T cell function by the V3 domain of the HIV-1 gp120 during antigen presentation

It was recently demonstrated that the semiconserved domain of the V3 region of the HIV-1 surface glycoprotein gp120 can induce an activation-apoptosis phenomenon to memory CD4+ cells from healthy individuals. Studying the eff ects of VS on the interaction of antigen presentation between monocyte-deri ved macrophages and resting memory CD4+ T cells, we observed that V3 affect s both cell, populations, Macrophages exposed to composite liposomes contai ning V3 on the surface and tetanus toroid (TT) as the recall antigen entrap ped in the aqueous phase (lipoV3/TT liposomes) were able to activate CD4+ T cells during primary stimulation, but not after restimulation nine days la ter. Unstimulated macrophages or macrophages exposed to soluble TT responde d to second stimuli, lipoV3/TT liposomes, and soluble TT in activating CD4 T cells. Soluble TT-activated CD4+ T cells could be restimulated by solubl e TT but not by lipoV3/TT liposomes, whereas lipoV3/TT liposome-activated C D4+ T cells became unresponsive to a second stimulus. These results show th at resting memory CD4+ cells activated by macrophages presenting the recall antigen together with V3 become unresponsive to restimulation, (C) 2001 Ac ademic Press.