Apoptosis induced in HIV-1-exposed, resting CD4+ T cells subsequent to signaling through homing receptors is Fas/Fas ligand-mediated

Jiaxiang Ji, Jenny J Y Chen, Vivian L. Braciale, Miles W. Cloyd

Research output: Contribution to journalArticle

12 Scopus citations

Abstract

The hallmark of HIV-1 disease is the gradual disappearance of CD4 + T cells from the blood. The mechanism of this depletion, however, is still unclear. Evidence suggests that lymphocytes die in lymph nodes, not in blood, and that uninfected bystander cells are the predominant cells dying. Our and others' previous studies showed that the lymph node homing receptor, CD62 ligand (CD62L), and Fas are up-regulated on resting CD4+ T cells after HIV-1 binding and that these cells home to lymph nodes at an enhanced rate. During the homing process, signals are induced through various homing receptors, which in turn, induced many of the cells to undergo apoptosis after they entered the lymph nodes. The purpose of this study was to determine how the homing process induces apoptosis in HIV-1-exposed, resting CD4+ T cells. We found that signaling through CD62L up-regulated FasL. This resulted in apoptosis of only HIV-1-presignaled, resting CD4+ T cells, not normal CD4+ T cells. This homing receptor-induced apoptosis could be blocked by anti-FasL antibodies or soluble Fas, demonstrating that the Fas-FasL interaction caused the apoptotic event.

Original languageEnglish (US)
Pages (from-to)297-305
Number of pages9
JournalJournal of Leukocyte Biology
Volume81
Issue number1
DOIs
StatePublished - Jan 2007

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Keywords

  • AIDS
  • Human
  • Lymphocytes

ASJC Scopus subject areas

  • Cell Biology

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