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Volume 9 Supplement 2

AIDS Vaccine 2012

  • Poster presentation
  • Open Access

Downregulation of the 5’-ectonucleotidase CD73 of CD8+ CTL of HIV infected patients correlates with immune activation and diminished IL-2 production

  • 2,
  • 1,
  • 2,
  • 2 and
  • 2
Retrovirology20129 (Suppl 2) :P261

  • Published:


  • Immune Activation
  • Irreversible Loss
  • Proliferation Study
  • Elite Controller
  • CD73 Downregulation


Chronic untreated HIV infection is immunologically characterized by irreversible loss of CD4+ T cells, general immune activation and CD4+ and CD8+ T cell dysfunction with diminished proliferative capacity. CD73 is an ectoenzyme (5'-ectonucleotidase) expressed on T cells converting 5'-AMP to adenosine, but there is additional evidence of ectonucleotidase-independent CD73 function. Altogether CD73 seems to play a role as a co-stimulatory molecule for T cell differentiation.


Peripheral blood of a large cohort of 103 HIV infected patients at different stages of HIV disease, including long-term nonprogressors and elite controllers, was analyzed by multicolour flow cytometry to determine the expression of CD73+ on CD8+ CTL, CD4+ T effector cells and Tregs.


Surprisingly CD73 was not expressed on human regulatory T cells regardless of the infection status. However we find high expression of CD8+ in healthy controls. In HIV infection, CD73 seems to be generally suppressed on CD8+ T cells, independent of their naive or memory subtype. We find significant correlation between downregulation of CD73 and viremia, and there is an inverse correlation with CD8+ immune activation. Elite controllers show comparable CD73 expression to healthy controls. First proliferation studies show that that HIV-specific CD8+ CD73- T cell population produces less IL-2 than their CD73+ counterparts.


CD73 is not expressed on human Tregs. CD73 downregulation of CD8+ T cells correlates with HIV disease progression. Further functional studies should look into the exact role of CD73 in HIV.

Authors’ Affiliations

Heinrich Pette Institute, Germany
University of Hamburg, Hamburg, Germany


© Toth et al; licensee BioMed Central Ltd. 2012

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.