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  • Meeting abstract
  • Open Access

Functional impairment of Tax-specific but not CMV-specific CTLs in a minor population of asymptomatic HTLV-1-carriers

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Retrovirology20118 (Suppl 1) :A101

  • Published:


  • Spastic Paraparesis
  • Minor Population
  • Asymptomatic Stage
  • Peptide Stimulation
  • Major Target Antigen

Human T-cell leukemia virus type 1 (HTLV-1) causes adult T-cell leukemia (ATL) and HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) in a small percentage of infected individuals. ATL is often associated with general immune suppression and an impaired HTLV-1-specific T cell response. We previously found that a small fraction of asymptomatic HTLV-1-carriers (AC) also showed impaired T cell responses against the major target antigen Tax. However, it is unclear whether the impaired HTLV-1-specific T cell response in these individuals is an HTLV-1-specific phenomenon, or merely reflects general immune suppression. In this study, we investigated the function of Tax-specific cytotoxic T lymphocytes (CTLs) using tetramers consisting of major CTL epitopes and HLA-A0201, A2402, or A1101 in various HTLV-1-infected individuals possessing these HLAs. Tax-specific CTLs were detected in 33.3% (n=7/21), 100% (n=18/18), and 86.4% (n=19/22) of chronic ATL (cATL) patients, HAM/TSP patients, and AC, respectively. Tax-specific CTLs of all HAM/TSP patients tested proliferated well in culture and produced IFN-γ when stimulated with Tax peptides, while Tax-specific CTLs detected in cATL patients did not. In ACs, the Tax-specific CTL responses were retained in most cases. However, Tax-specific CTLs in one AC hardly produced IFN-γ and failed to proliferate or express a degranulation (CD107a) marker upon Tax peptide stimulation. In contrast, cytomegalovirus (CMV) pp65-specific CTLs in the same donor could be fully activated by pp65 peptide stimulation. These findings indicated that HTLV-1-specific T cell function is impaired in a limited population in an HTLV-1-specific manner during an asymptomatic stage.

Authors’ Affiliations

Department of Immunotherapeutics, Tokyo Medical and Dental University, Tokyo 113-8519, Japan
Department of Hematology, Imamura Bun-in Hospital, Kagoshima, Japan
Division of Hematology, Department of Internal Medicine, Kinki University School of Medicine, Osaka, Japan
Department of Molecular Medical Science, Institute of Medical Science, St. Marianna University School of Medicine, Kawasaki, Japan
Department of Hematology, National Kyushu Cancer Center, Fukuoka, Japan
Institute for Clinical Research, National Kyushu Cancer Center, Fukuoka, Japan
Laboratory of Tumor Cell Biology, Department of Medical Genome Science, Graduate School of Frontier Sciences, The University of Tokyo, Tokyo, Japan


© Hasegawa 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 (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.