Expression of CD10 by Human T Cells That Undergo Apoptosis Both In Vitro and In Vivo

Abstract

This study shows that human postthymic T cells express CD10 when undergoing apoptosis, irrespective of the signal responsible for initiating the apoptotic process. Cells from continuous T-cell lines did not normally express CD10, but became CD10+ when induced into apoptosis by human immunodeficiency virus (HIV) infection and exposure to CD95 monoclonal antibody, etoposide, or staurosporin. Inhibitors of caspases blocked apoptosis and CD10 expression. Both CD4+ and CD8+ T cells purified from normal peripheral blood expressed CD10 on apoptotic induction. CD10 was newly synthesized by the apoptosing cells because its expression was inhibited by exposure to cycloheximide and CD10 mRNA became detectable by reverse transcription-polymerase chain reaction in T cells cultured under conditions favoring apoptosis. To show CD10 on T cells apoptosing in vivo, lymph node and peripheral blood T cells from HIV+ subjects were used. These suspensions were composed of a substantial, although variable, proportion of apoptosing T cells that consistently expressed CD10. In contrast, CD10+ as well as spontaneously apoptosing T cells were virtually absent in peripheral blood from normal individuals. Collectively, these observations indicate that CD10 may represent a reliable marker for identifying and isolating apoptosing T cells in vitro and ex vivo and possibly suggest novel functions for surface CD10 in the apoptotic process of lymphoid cells.

Retinoic Acid Improves the Recovery of Replication-Competent Virus from Latent SIV Infected Cells

“…In agreement with our findings, Ding et al, also reported the use of immobilized CD3 beads followed by treatment with RA that generated a similar distribution of α4β7 + CD4 + T cell subsets that was characterized by a predominantly naive CD4 + T cell phenotype [57]. Earlier reports by Cutrona et al indicated that CD10 expression on T cells could be used to reliably identify cells undergoing apoptosis during cell division [58,59]. Unsurprisingly, we observed elevated expression of CD10 within the TEMRA CD4 + T cells and an increasing trend within the EM CD4 + T cells of RA-induced α4β7 + CD4 + T cells hence accounting for their rapid turnover.…”