International Immunology, Vol 9, 1367-1374, Copyright © 1997 by Oxford University Press
H Suzuki, A Hayakawa, D Bouchard, I Nakashima and TW Mak
Mice lacking the IL-2 receptor beta chain (IL-2R beta) exhibit an
autoimmune reaction characterized by generalized T cell activation,
production of autoantibodies, myeloproliferation and severe anemia. T cells
of IL-2R beta-/- mice were examined to elucidate the mechanism responsible
for their abnormal activation and to determine how such abnormal activation
might affect other cell lineages. Elevated levels of IgG, IgE and
autoantibodies in IL-2R beta-/- mice were found to be associated with
activated CD4+ T cells which secreted elevated levels of IL-4. Thymocytes
in IL-2R beta-/- mice showed normal negative and positive selection
patterns when analyzed in transgenic mice bearing a TCR specific for HY
antigen, suggesting that neither IL-2 nor IL-15 is essential for thymic
selection. Peripheral T cells in IL-2R beta- deficient mice underwent
normal programmed cell death in response to staphylococcal enterotoxin B
superantigen, in contrast to cells from mice deficient for either IL-2 or
IL-2R alpha. Activated T cells in IL- 2R beta-deficient mice expressed
normal levels of Fas antigen and underwent normal apoptosis in response to
induction with anti-Fas mAb. Thus, the accumulation of activated T cells in
IL-2R beta-/- mice does not appear to be derived from abnormalities in
either thymic selection or Fas-mediated apoptosis.
ARTICLES
Normal thymic selection, superantigen-induced deletion and Fas-mediated apoptosis of T cells in IL-2 receptor beta chain-deficient mice
Department of Immunology, Nagoya University, School of Medicine, Japan.
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