Blockade of IL-2 Receptor Suppresses HTLV-I and IFN-ﾎｳ Expression in Patients with HTLV-I-Associated Myelopathy/Tropical Spastic Paraparesis

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概要

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• Objective: Th1 activation based on a high HTLV-I proviral load is one of the characteristic immunological abnormalities in the peripheral blood lymphocytes of patients with HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP). To clarify the cause of this abnormality with the potential to be one of the therapeutic targets, we analyzed the involvement of interleukin-2 (IL-2)/IL-2 receptor (IL-2R) signaling in HTLV-I and interferon-γ (IFN-γ), which is a representative Th1 cytokine, expression in peripheral blood CD4+ T cells from HAM/TSP patients. Patients and Methods: Twelve patients with HAM/TSP were included in the study. After the peripheral blood CD4+ T cells were treated in cultures under the presence of each anti-IL-2Rα, β,and γ blocking antiboby for 48 hours, both HTLV-I p19 antigen and IFN-γ levels in the culture supernatants were measured using ELISA methods. To check the influence on cell proliferation under these culture conditions, the numbers of viable cells were simultaneously determined by MTS assay. Results: Treatment with anti-IL-2Rα blocking antibody, but not anti-IL-2Rβ or anti-IL-2Rγ blocking antibody, suppressed HTLV-I p19 antigen expression levels. In addition, treatment with all types of anti-IL-2R blocking antibodies also suppressed IFN-γ expression levels. All of the types of anti-IL-2R blocking antibodies did not inhibit the proliferation. Conclusion: These results indicate that IL-2/IL-2R signaling is involved in HTLV-I and IFN-γ expression on peripheral blood CD4+ T cells from HAM/TSP patients, suggesting that the interruption of this signaling has therapeutic potential against HAM/TSP in patients with the focus on the down-regulation of Th1 activation based on a high HTLV-I proviral load in the peripheral blood.

著者

• Nakamura Tatsufumi

  Department Of Applied Physics Waseda University

• KOHNO Shigeru

  Department of Internal Medicine, Nagasaki University School of Medicine

• Eguchi Katsumi

  First Department Of Internal Medicine Graduate School Of Biochemical Sciences Nagasaki University

• NISHIURA YOSHIHIRO

  First Department of Internal Medicine, Graduate School of Biomedical Sciences, Nagasaki University

• Fukushima Naomi

  Department Of Molecular Microbiology And Immunology Graduate School Of Biomedical Sciences Nagasaki

• Nakamura Tatsufumi

  Department of Molecular Microbiology and Immunology, Graduate School of Biomedical Sciences, Nagasaki University

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