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Deregulated T cell activation and autoimmunity in mice lacking interleukin-2 receptor beta.

In mice lacking the interleukin-2 receptor beta chain (IL-2R beta), T cells were shown to be spontaneously activated, resulting in exhaustive differentiation of B cells into plasma cells and the appearance of high serum concentrations of immunoglobulins G1 and E as well as autoantibodies that cause hemolytic anemia. Marked infiltrative granulocytopoiesis was also apparent, and the animals died after about 12 weeks. Depletion of CD4+ T cells in mutant mice rescued B cells without reversion of granulocyte abnormalities. T cells did not proliferate in response to polyclonal activators, nor could antigen-specific immune responses be elicited. Thus, IL-2R beta is required to keep the activation programs of T cells under control, to maintain homeostasis, and to prevent autoimmunity.

Pubmed ID: 7770771


  • Suzuki H
  • K√ľndig TM
  • Furlonger C
  • Wakeham A
  • Timms E
  • Matsuyama T
  • Schmits R
  • Simard JJ
  • Ohashi PS
  • Griesser H


Science (New York, N.Y.)

Publication Data

June 9, 1995

Associated Grants


Mesh Terms

  • Animals
  • Autoantibodies
  • Autoimmunity
  • B-Lymphocytes
  • CD4-Positive T-Lymphocytes
  • Female
  • Heterozygote
  • Homozygote
  • Lymph Nodes
  • Lymphocyte Activation
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Nude
  • Mutagenesis, Insertional
  • Myeloproliferative Disorders
  • Receptors, Interleukin-2
  • Signal Transduction
  • T-Lymphocytes
  • T-Lymphocytes, Cytotoxic