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Molecular and Cellular Biology, July 2006, p. 5214-5225, Vol. 26, No. 14
0270-7306/06/$08.00+0     doi:10.1128/MCB.00087-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

3BP2 Deficiency Impairs the Response of B Cells, but Not T Cells, to Antigen Receptor Ligation

Division of Immunology,¹ Ina Sue Perlmutter Laboratory, Children's Hospital and Departments of Pediatrics and Medicine, Harvard Medical School, Boston, Massachusetts 02115²

Received 13 January 2006/ Returned for modification 20 February 2006/ Accepted 19 April 2006

The adapter protein 3BP2 is expressed in lymphocytes; binds to Syk/ZAP-70, Vav, and phospholipase C- (PLC-); and is thought to be important for interleukin-2 gene transcription in T cells. To define the role of 3BP2 in lymphocyte development and function, we generated 3BP2-deficient mice. T-cell development, proliferation, cytokine secretion, and signaling in response to T-cell receptor (TCR) ligation were all normal in 3BP2^–/– mice. 3BP2^–/– mice had increased accumulation of pre-B cells in the bone marrow and a block in the progression of transitional B cells in the spleen from the T1 to the T2 stage, but normal numbers of mature B cells. B-cell proliferation, cell cycle progression, PLC-2 phosphorylation, calcium mobilization, NF-ATp dephosphorylation, and Erk and Jnk activation in response to B-cell receptor (BCR) ligation were all impaired. These results suggest that 3BP2 is important for BCR, but not for TCR signaling.

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