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J. Exp. Med.,
Volume 187, Number 7, April 6, 1998 1081-1091
By
From the * Department of Immunology; the Mutations in the tyrosine kinase, Btk, result in a mild immunodeficiency in mice (xid). While
B lymphocytes from xid mice do not proliferate to anti-immunoglobulin (Ig), we show here
induction of the complete complement of cell cycle regulatory molecules, though the level of
induction is about half that detected in normal B cells. Cell cycle analysis reveals that anti-Ig
stimulated xid B cells enter S phase, but fail to complete the cell cycle, exhibiting a high rate of
apoptosis. This correlated with a decreased ability to induce the anti-apoptosis regulatory protein, Bcl-xL. Ectopic expression of Bcl-xL in xid B cells permitted anti-Ig induced cell cycle
progression demonstrating dual requirements for induction of anti-apoptotic proteins plus cell
cycle regulatory proteins during antigen receptor mediated proliferation. Furthermore, our results link one of the immunodeficient traits caused by mutant Btk with the failure to properly
regulate Bcl-xL.
Department of Human Immunology; and the § Department of Cell Signaling, DNAX Research Institute, Palo Alto, California 94304; the Department of Medicine, University of Minnesota, Minneapolis, Minnesota 55455; the ¶ University
of Michigan Medical School, Ann Arbor, Michigan 48109
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