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Retrovirology

Open Access

Reduced Tim-3 expression on HTLV-I Tax-specific cytotoxic T lymphocytes in HTLV-I infection

  • Nashwa H Abdelbary1,
  • Hazem M Abdullah1,
  • Toshio Matsuzaki2,
  • Daisuke Hayashi2,
  • Yuetsu Tanaka3,
  • Hiroshi Takashima2,
  • Shuji Izumo1 and
  • Ryuji Kubota1Email author
Retrovirology20118(Suppl 1):A112

https://doi.org/10.1186/1742-4690-8-S1-A112

Published: 6 June 2011

T-cell immunoglobulin and mucin domain-containing molecule-3 (Tim-3) and programmed cell death-1 (PD-1) are T-cell exhaustion molecules. We investigated the expression of Tim-3 and PD-1 in HTLV-I infection. Tim-3 expression, but not PD-1 expression, was reduced on CD4+ and CD8+ T cells of HAM/TSP patients and HTLV-I carriers as compared to healthy controls. Tim-3 expression was also reduced in HTLV-I Tax-specific cytotoxic T lymphocytes (CTLs) as compared to cytomegalovirus-specific CTLs. Tim-3+, but not PD-1+, Tax-specific CTLs produced less interferon-γ and exhibited low cytolytic activity. However, we observed no difference in the expression of Tim-3 or cytolytic activity between Tax-specific CTLs of HAM/TSP patients or carriers. Moreover, HTLV-I-infected CD4+ T cells showed decreased Tim-3 expression. The decreased expression of Tim-3 in HTLV-I infection is a marked contrast to other chronic viral infections such as HIV and HCV infection, where Tim-3 expression is increased in T cells, including the virus-specific CTLs. In HTLV-I infection, CTL response may not be negatively regulated by Tim-3. Rather, immune cells such as HTLV-I-specific CTLs may be resistant to cell death through the Tim-3/galectin-9 pathway. In summary, our data suggest that Tim-3 expression is reduced in HTLV-I infection and that a high number of Tim-3- HTLV-I-specific CTLs preserves their cytolytic activity, thereby controlling viral replication.

Authors’ Affiliations

(1)
Center for Chronic Viral Diseases, Kagoshima University, Kagoshima, Japan
(2)
Department of Neurology and Geriatrics, Kagoshima University, Kagoshima, Japan
(3)
Department of Immunology, University of the Ryukyus, Okinawa, Japan

Copyright

© Abdelbary et al; licensee BioMed Central Ltd. 2011

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 (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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