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.
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