Transgene expression of bcl-x(L) permits anti-immunoglobulin (Ig)- induced proliferation in xid B cells

Nanette Solvason, Wei Wei Wu, Nisha Kabra, Fridjtof Lund-Johansen, Maria Grazia Roncarolo, Timothy W. Behrens, Didier A M Grillot, Gabriel Nunez, Emma Lees, Maureen Howard

Research output: Contribution to journalArticlepeer-review

Abstract

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-X(L). Ectopic expression of Bcl-X(L) 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-x(L).

Original languageEnglish
Pages (from-to)1081-1091
Number of pages11
JournalJournal of Experimental Medicine
Volume187
Issue number7
DOIs
Publication statusPublished - Apr 6 1998

ASJC Scopus subject areas

  • Immunology

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