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  • Meeting abstract
  • Open Access

The plasticity of HTLV-1 infected CD4+CD25+CCR4+ T-cells through HTLV-1 tax in HAM/TSP

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Retrovirology20118 (Suppl 1) :A104

  • Published:


  • mRNA Expression
  • Disease Severity
  • Proinflammatory Cytokine
  • Inflammatory Disease
  • Chronic Inflammation

Recently, it has become increasingly clear that some committed effecter and regulatory T (Treg) cells are not stable, and the plasticity of committed T-cells may be related to autoimmunity and inflammatory disease. However, the environmental (extrinsic) molecules that allow for plasticity have not yet been clearly understood.

In Human T-lymphotropic virus type 1 (HTLV-1) associated myelopathy /tropical spastic paraparesis (HAM/TSP), the pathogenesis is known as HTLV-1 infected CD4+ T-cells triggered hyper immune response, which leads to chronic inflammation of the central nervous system. In our previous study, we demonstrated that the majority of CD4+CD25+CCR4+ T-cells were infected with HTLV-1 and that this T-cell subset was increased in HAM/TSP. Although CD4+CD25+CCR4+ T-cells of healthy condition include suppressive T cell subsets such as Treg and Th2, this T-cell subset becomes Th1-like cells with overproduction of IFN-γ in HAM/TSP patients (PLoS ONE 2009). Since HTLV-1 tax is known to up-regulate the expression of several proinflammatory cytokines, and importantly, the level of HTLV-1 tax mRNA expression is reported to correlate with disease severity in HAM/TSP patients, we hypothesize that HTLV-1 tax may convert HTLV-1 infected T-cells into abnormal IFN-γ producing Th1-like T-cells in HAM/TSP. In this study, we present the molecular mechanisms underlying the plasticity of HTLV-1 infected CD4+CD25+CCR4+ T-cells through HTLV-1 tax.

Authors’ Affiliations

Department of Molecular Medical Science, Institute of Medical Science, St. Marianna University School of medicine, Kawasaki, Japan
Department of Hematology, Imamura Bun-in Hospital, Kagoshima, Japan
Department of Immunotherapeutics, Tokyo Medical and Dental University, Graduate School, Tokyo, Japan
Department of Molecular Microbiology and Immunology, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan
Department of Immunology, Graduate School of Medicine, University of the Ryukyus, Okinawa, Japan
Viral Immunology Section, Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA


© Araya 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.