During signal transduction through the B cell antigen receptor (BCR), several signaling elements are brought together by the adaptor protein SLP- 65. We have investigated the role of SLP-65 in B cell maturation and function in mice deficient for SLP-65. While the mice are viable, B cell development is affected at several stages. SLP-65-deficient mice show increased proportions of pre-B cells in the bone marrow and immature B cells in peripheral lymphoid organs. B1 B cells are lacking. The mice show lower IgM and IgG3 serum titers and poor IgM but normal IgG immune responses. Mutant B cells show reduced Ca2+ mobilization and reduced proliferative responses to B cell mitogens. We conclude that while playing an important role, SLP65 is not always required for signaling from the BCR.
CITATION STYLE
Jumaa, H., Wollscheid, B., Mitterer, M., Wienands, J., Reth, M., & Nielsen, P. J. (1999). Abnormal development and function of B lymphocytes in mice deficient for the signaling adaptor protein SLP-65. Immunity, 11(5), 547–554. https://doi.org/10.1016/S1074-7613(00)80130-2
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