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Spontaneous T Cell Proliferation and Release of Soluble Interleukin-2 Receptors in Patients with HTLV-I-Associated Myelopathy
Mitsuhiro Matsumoto
Mitsuhiro Matsumoto
Institute for Medical Immunology, Kumamoto University Medical School, Kumamoto, Japan
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Mineharu Sugimoto
Mineharu Sugimoto
Institute for Medical Immunology, Kumamoto University Medical School, Kumamoto, Japan
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Hironori Nakashima
Hironori Nakashima
Institute for Medical Immunology, Kumamoto University Medical School, Kumamoto, Japan
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Fumiya Imamura
Fumiya Imamura
Institute for Medical Immunology, Kumamoto University Medical School, Kumamoto, Japan
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Osamu Kawano
Osamu Kawano
Institute for Medical Immunology, Kumamoto University Medical School, Kumamoto, Japan
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Ehchiro Uyama
Ehchiro Uyama
Institute for Medical Immunology, Kumamoto University Medical School, Kumamoto, Japan
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Kiyoshi Takatsu
Kiyoshi Takatsu
Institute for Medical Immunology, Kumamoto University Medical School, Kumamoto, Japan
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Shukuro Araki
Shukuro Araki
Institute for Medical Immunology, Kumamoto University Medical School, Kumamoto, Japan
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Patients with human T lymphotropic virus type I (HTLV-I)-associated myelopathy (HAM) show increased serum levels of soluble interleukin-2 receptors (sIL-2R), a marker of T cell activation. We found that peripheral blood lymphocytes from HAM patients proliferated spontaneously and released sIL-2R when cultured in vitro. Spontaneous proliferation was observed in T cell populations (both CD4+ cells and CD8+ cells), but not in B cell-rich populations or monocyte-rich populations. There was a significant increase of IL-2 activity in the culture supernatants of peripheral blood mononuclear cells (PBMC) after 2–3 days cultivation. On the other hand, sIL-2R concentrations in the supernatants were much higher after 5 days of cultivation. Such spontaneous T lymphocytic proliferation and release of sIL-2R were also found in non-HAM HTLV-I carriers, but not as intensely as in HAM patients. HTLV-I infection causes T cell activation to release IL-2 and sIL-2R; such T cell responses may play a role in the pathogenesis of HTLV-I-associated myelopathy.
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