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Volume 9 Supplement 2

AIDS Vaccine 2012

  • Poster presentation
  • Open Access

Highly expression of Tim-3 on HIV-specific T cells associated with disease progression and T-cell exhaustion in HIV-1 infected Chinese

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Retrovirology20129 (Suppl 2) :P270

  • Published:


  • Cellular Immune Response
  • Primary Infector
  • Blocking Effect
  • Immune Regulation
  • Intracellular Cytokine Staining


The exact mechanism of T-cell exhaustion remains to be defined during HIV-1 infection. Recent studies suggest that the inhibitory receptor T-cell immunoglobulin domain and mucin domain 3(Tim-3) may play an important role in the exhaustion of HIV-specific T cells.


72 HIV-1 infected individuals with different disease outcomes were recruited in this study. Tim-3 expression and the profile of cellular immune response were measured by using Multicolor Intracellular Cytokine Staining (ICS) assay. Association between Tim-3 expression levels and disease progression was analyzed. And the potential role of Tim-3 on immune regulation during HIV-1 infection was investigated through assessment of CTL response with frequencies of Tim-3 expression and blocking effect.


Tim-3 was found to be highly expressed on HIV-specific CD4+ T cells and CD8+ T cells, especially in primary infectors and AIDS patients. The frequencies of Tim-3 expression correlate with disease progression. The level of Tim-3 expression was related with cytokines production and blockade of Gal-9/TIM-3 signaling partially restored the ability of HIV-specific T cells to secrete cytokines in vitro.


The frequencies of Tim-3 expression correlate with disease progression in HIV-1 infected individuals and manipulating Gal-9/TIM-3 signaling pathway may provide a novel therapeutic measure to control HIV-1 replication.

Authors’ Affiliations

National Center for AIDS Control and Prevention, China CDC, Beijing, China


© Liu 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.