Administration of anti-interleukin-2 receptor α antibody in vivo induces localized autoimmune disease

Authors

  • Osamu Taguchi,

    Corresponding author
    1. Laboratory of Experimental Pathology, Aichi Cancer Center Research Institute, Nogoya, Japan
    • Laboratory of Experimental Pathology, Aichi Cancer Center Research Institute, Chikusaku, Nagoya 464, Japan
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  • Toshitada Takahashi

    1. Laboratory of Immunology, Aichi Cancer Center Research Institute, Nagoya, Japan
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Abstract

Neonatal thymectomy (Tx) of mice at day 3 after birth (Tx-3), but not day 7 (Tx-7), induces organ-localized autoimmune diseases such as oophoritis and gastritis. Lesions in Tx-3 mice can be prevented by injection of splenic CD4+ cells from syngeneic normal mice, and this CD4+ population with suppressor activity is activated extrathymically by self antigens. Since it is speculated that these CD4+ T suppressor cells (Ts) express the interleukin-2 receptor (IL-2R) as an activated T cell population, an attempt was made to eliminate these Ts from the developing immune system of Tx-7 mice and normal mice by i.p. injection of anti-IL-2Rα monoclonal antibodies. Interestingly, organ-localized autoimmune disease with quite similar characteristics to those observed after neonatal Tx developed in not only Tx-7 mice, but also normal mice. The results thus indicate that CD4+ cells expressing IL-2Rα play an important role, as Ts in the periphery, in maintaining immune tolerance.

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