作者: Benjamin Sadlack , Jürgen Löhler , Hubert Schorle , Gabriele Klebb , Hildegard Haber
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摘要: Interleukin-2-deficient mice (IL-2-/-) crossed to a BALB/c genetic background develop lymphoproliferative syndrome with severe hemolytic anemia and die within 5 weeks of age. The presence autoantibodies various specificities inflammatory lesions in several organs are indicative generalized auto-immune disease. No alterations the immune system were observed 6-day-old animals, but 10-day-old already showed an increased proliferation polyclonal activation lymphocytes. treatment IL-2-/- anti-gp39(CD40L) antibody prevented disease indicated that appearance activated CD4- T cells (CD44high, CD69-) represents first alteration mice. Collectively, our results suggest essential role IL-2 vivo, which is not compensated by other cytokines, maintenance self tolerance.