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Title: Abnormal development and function of B lymphocytes in mice deficient for the signaling adaptor protein SLP-65. Author: Jumaa H, Wollscheid B, Mitterer M, Wienands J, Reth M, Nielsen PJ. Journal: Immunity; 1999 Nov; 11(5):547-54. PubMed ID: 10591180. Abstract: 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, SLP-65 is not always required for signaling from the BCR.[Abstract] [Full Text] [Related] [New Search]