The Interaction of Recombinant IL-2 with Human Resting Lymphocytes

J-STAGE
  • ISEKI Rieko
    Department of Dermatology, Nagoya University School of Medicine
  • KOIDE Yukio
    Department of Microbiology and Immunology, Hamamatsu University School of Medicine
  • UEDA Ryuzo
    Laboratory of Chemotherapy, Aichi Cancer Center Research Institute
  • KONDO Nobuo
    Central Research Laboratories, Ajinomoto Co., Inc.
  • HAMURO Junji
    Central Research Laboratories, Ajinomoto Co., Inc.
  • YOSHIDA Takato O.
    Department of Microbiology and Immunology, Hamamatsu University School of Medicine

抄録

Several lines of evidence suggest that subsets of resting lymphocytes naturally express interleukin-2 receptors (IL-2•R). Recombinant IL-2 (rIL-2) induced the enhancement of natural killer (NK) activity, the generation of activated killer (AK) cells, the proliferation of resting lymphocytes, and the production of interferon-γ (IFN-γ) in lymphocyte cultures. The subsets of lymphocytes mediating these responses appeared to be heterogeneous, but reside predominantly in nylon wool-passed non-T, non-B cells ("null cells" or T3- cells); in response to rIL-2, only Leu11+T3- cells showed enhanced NK activity, and both Leu11+T3- and Leu11-T3- cells showed predominantly AK activity, proliferation and production of IFN-γ. These findings suggest that the T3- fraction (null cell fraction) contains predominantly cells expressing IL-2•R at the resting state. Unlike the case with activated T cells, however, none of these responses was blocked by any of three monoclonal antibodies to IL-2•R, including anti-Tac antibody at any dilution. These results indicate that IL-2•R on the resting T3- cells possess unique biological features compared to those on activated T or B cells. A most likely explanation is that T3- cells possess higher affinity IL-2•R than activated T or B cells. Other possibilities are also discussed.

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