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  • Meeting abstract
  • Open Access

Possibility of γδ T cell immunotherapy for HTLV-1-infected individuals

  • 1,
  • 2,
  • 1,
  • 2,
  • 1,
  • 3,
  • 4 and
  • 1Email author
Retrovirology20118 (Suppl 1) :A109

https://doi.org/10.1186/1742-4690-8-S1-A109

  • Published:

Keywords

  • Infectious Disease
  • Protective Effect
  • Cancer Research
  • Cytotoxic Activity
  • Protective Role

γδ T cells, a small subset of T lymphocytes, are involved in innate immunity. It has been demonstrated that γδ T cells have cytotoxic activities against cells infected with a variety of viruses. However, there is little evidence suggesting a cytotoxic activity of γδ T cells against HTLV-1-infected cells. Therefore, we investigated whether γδ T cells play a protective role in the defense against HTLV-1.

Using PBMCs from asymptomatic carriers (ACs) and HAM/TSP patients, we assayed the frequency of CD3+Vγ9+ (γδ T) cells and the correlation between its frequency and the HTLV-1 load. The frequency of γδ T cells was significantly decreased in HAM/TSP patients compared with that in ACs. The frequency of γδ T cells was inversely correlated with the proviral load. These results suggest that γδ T cells have a protective effect on HTLV-1-infected individuals. Next, CD3+Vγ9+ cells and CD3+Vγ9- cells were separated from PBMCs of HTLV-1-infected persons by FACS and the proviral load of each population was quantified by real-time PCR. The proviral load in γδ T cells was markedly lower than that in CD3+ lacking γδ T cells. Furthermore, we cultured PBMCs from HTLV-1-infected individuals in the presence of IL-2 and zoledronate. In some cases, the majority of cells contained in these cultures became γδ T cells and the proviral load was markedly decreased. The cultured PBMCs showed strong cytotoxic activities against a HTLV-1-infected cell line as well as an ATL cell line. These results raise the possibility of γδ T cell immunotherapy in HTLV-1-infected individuals.

Authors’ Affiliations

(1)
Institute of Medical Science, St. Marianna University School of Medicine, Kawasaki, Japan
(2)
Medinet Medical Institute, MEDINET Co. Ltd., Tokyo, Japan
(3)
Department of Hematology, Imamura Bun-in Hospital, Kagoshima, Japan
(4)
Institute for Genetic Medicine Research Section of Pathophysiology, Hokkaido University, Hokkaido, Japan

Copyright

© Sato 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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