Deregulated T Cell Activation and Autoimmunity in Mice Lacking Interleukin-2 Receptor β

• Haruhiko Suzuki

  Amgen Institute, Toronto, Ontario, Canada.

• Thomas M. Kündig

  Ontario Cancer Institute, Departments of Immunology and Medical Biophysics, University of Toronto, Toronto, Ontario M4X 1 K9, Canada.

• Caren Furlonger

  Wellesley Hospital Research Institute, Toronto, Ontario M4Y 1,J3, Canada.

• Andrew Wakeham

  Amgen Institute, Toronto, Ontario, Canada.

• Emma Timms

  Amgen Institute, Toronto, Ontario, Canada.

• Toshifumi Matsuyama

  Amgen Institute, Toronto, Ontario, Canada.

• Rudolf Schmits

  Amgen Institute, Toronto, Ontario, Canada.

• John J. L. Simard

  Amgen Institute, Toronto, Ontario, Canada.

• Pamela S. Ohashi

  Ontario Cancer Institute, Departments of Immunology and Medical Biophysics, University of Toronto, Toronto, Ontario M4X 1 K9, Canada.

• Henrik Griesser

  Department of Pathology, University of Toronto, Toronto, Ontario M4X 1 K9, Canada.

• Tadatsugu Taniguchi

  Institute for Molecular and Cellular Biology, Osaka University, Yamada-oka 1-3, Suita-shi, Osaka 565, Japan.

• Christopher J. Paige

  Wellesley Hospital Research Institute, Toronto, Ontario M4Y 1,J3, Canada.

• Tak W. Mak

  Amgen Institute, Toronto, Ontario, Canada.

Abstract

In mice lacking the interleukin-2 receptor β chain (IL-2Rβ), 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-2Rβ is required to keep the activation programs of T cells under control, to maintain homeostasis, and to prevent autoimmunity.

Journal

• Science

  Science 268 (5216), 1472-1476, 1995-06-09

  American Association for the Advancement of Science (AAAS)

Keywords

• Multidisciplinary

Details

• CRID: 1360574095632223872
• NII Article ID: 80008363217
• DOI: 10.1126/science.7770771
• ISSN: 10959203
• ISSN: 00368075
• Web Site: https://www.science.org/doi/pdf/10.1126/science.7770771
• Data Source:
  • Crossref
  • CiNii Articles