A Novel Mechanism of CD4 Lymphocyte Depletion Involves Effects of HIV on Resting Lymphocytes: Induction of Lymph Node Homing and Apoptosis Upon Secondary Signaling Through Homing Receptors

摘要: Recently, we reported that abortive HIV infection of resting human T lymphocytes up-regulated expression CD62L, the receptor for homing to lymph nodes (LNs), and enhanced these cells from blood into LNs (Wang et al., 1997, Virology 228:141). This suggested HIV-induced (which comprise >98% all lymphocytes) may be a major mechanism reduction CD4+ in infected individuals. also could partially responsible lymphadenopathy often develops at same time are disappearing blood. In this study, show secondary signaling through receptors (CD62L, CD44, CD11a) abortively induced apoptosis. These signals would occur as home LNs. Apoptosis did not after some other (CD26, CD4, CD45, HLA class I) or HIV-exposed CD8+ signaled receptors. findings indicate results death many cells. was confirmed SCID mice were i.v. injected with lymphocytes. Thus, effects upon binding lymphocytes, which permissive replication, significantly contribute their depletion vivo. offer an explanation bystander effect observed AIDS patients, whereby making virus dying.