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CD8 memory T-cell differentiation during HIV infection: the role of RUNX3, Eomes, and T-bet transcription factors and their impact on CD127 expression

Wednesday, October 26, 2011 — Poster Session IV

2:00 p.m. – 4:00 p.m.

Natcher Conference Center




  • R Hasley
  • C Hong
  • T Friesen
  • C Wilhelm
  • Y Nakamura
  • G Kim
  • J Park
  • M Sneller
  • G Roby
  • C Rehm
  • C Lane
  • M Catalfamo


Immune activation plays an important role in HIV pathogenesis, and differentially affects CD4 and CD8 T cell pools. While there is a depletion of CD4 T cells, there is an expansion of CD8 T cells, specifically with a memory-like phenotype and CD127low expression. Survival of memory CD8 T cells is dependent on IL-7 signaling, therefore we hypothesized that in the context of HIV infection, memory CD8 T cells may not be able to undergo homeostatic proliferation and their survival and development is impaired due to the loss of CD127. In the present work, we studied the T-box transcription factors T-bet and Eomes, which govern the differentiation of effector versus memory CD8 T cells respectively, and the dynamics of CD127 and RUNX3 during HIV infection. We found that the inflammatory environment maintained by HIV-RNA levels favors expression of T-bet and Eomes concomitant to CD127 repression (R=-0.7194, p<0.0001). In patients with viral loads >50 copies/ml, memory CD8 T cells were CD127lowEomes+T-bethigh; however, in treated patients, T-bet expression decreased, and memory CD8 T cells were CD127highEomes+T-betlow. These data provide new evidence for the development of long-lived memory CD8 T cells in the context of chronic HIV infection and its importance in vaccine development.

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