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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adaptor Proteins, Signal Transducing
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Animals
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Antibody Formation
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B-Lymphocyte Subsets
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B-Lymphocytes / immunology
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B-Lymphocytes / pathology*
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Bone Marrow / pathology
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Calcium Signaling
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Carrier Proteins / genetics
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Carrier Proteins / metabolism
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Carrier Proteins / physiology*
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Cell Differentiation
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Cells, Cultured
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Flow Cytometry
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Immunologic Deficiency Syndromes / genetics*
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Lymphocyte Activation / physiology*
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Lymphocyte Count
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Lymphoid Tissue / pathology
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Mice
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Mice, Knockout
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Mitogens / pharmacology
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Phosphoproteins*
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Phosphorylation
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Protein Processing, Post-Translational / immunology*
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Protein-Tyrosine Kinases / metabolism
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Receptors, Antigen, B-Cell / immunology*
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Signal Transduction / immunology*
Substances
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Adaptor Proteins, Signal Transducing
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B cell linker protein
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Carrier Proteins
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Mitogens
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Phosphoproteins
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Receptors, Antigen, B-Cell
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Protein-Tyrosine Kinases