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Blood, 15 September 2005, Vol. 106, No. 6, pp. 2105-2112.
Prepublished online as a Blood First Edition Paper on May 5, 2005; DOI 10.1182/blood-2004-04-1248.
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Submitted April 2, 2004
Accepted February 1, 2005
Bcl10 can promote survival of antigen-stimulated B lymphocytes
Maoxin T Tian, Gabriel Gonzalez, Barbara Scheer, and Anthony L DeFranco*
G.W. Hooper Foundation & Department of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA, USA
* Corresponding author; email: defranco{at}cgl.ucsf.edu.
To understand the nature of negative responses through the B cell antigen receptor (BCR), we have screened an expression cDNA library for ability to block BCR-induced growth arrest and apoptosis in the immature B cell line, WEHI-231. We isolated multiple copies of full-length, unmutated Bcl10, a signaling adaptor molecule encoded by a gene found to translocate to the IgH locus in some MALT lymphomas. A conditionally active form of Bcl10 protected WEHI-231 cells from BCR-induced apoptosis upon activation. Induction of Bcl10 activity caused rapid activation of NF- B and JNK, but not activation of ERK or p38 MAP kinases. These results support genetic and biochemical experiments which have implicated Bcl10 and its binding partners Carma-1 and MALT1 in mediating the ability of the BCR to activate NF-B. The ability of Bcl10 expression to prevent BCR-induced growth arrest and apoptosis of WEHI-231 cells was dependent on NF-B activation. Finally, overexpression of Bcl10 in primary B cells activated ex vivo promoted the survival of these cells after removal of activating stimuli. Taken together these results support the hypothesis that enhanced BCL10 expression caused by translocation to the IGH locus can promote formation of MALT lymphomas.
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