Abnormal development and function of B lymphocytes in mice deficient for the signaling adaptor protein SLP-65

Immunity. 1999 Nov;11(5):547-54. doi: 10.1016/s1074-7613(00)80130-2.


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

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing
  • Animals
  • Antibody Formation
  • B-Lymphocyte Subsets
  • B-Lymphocytes / immunology
  • B-Lymphocytes / pathology*
  • Bone Marrow / pathology
  • Calcium Signaling
  • Carrier Proteins / genetics
  • Carrier Proteins / metabolism
  • Carrier Proteins / physiology*
  • Cell Differentiation
  • Cells, Cultured
  • Flow Cytometry
  • Immunologic Deficiency Syndromes / genetics*
  • Lymphocyte Activation / physiology*
  • Lymphocyte Count
  • Lymphoid Tissue / pathology
  • Mice
  • Mice, Knockout
  • Mitogens / pharmacology
  • Phosphoproteins*
  • Phosphorylation
  • Protein Processing, Post-Translational / immunology*
  • Protein-Tyrosine Kinases / metabolism
  • Receptors, Antigen, B-Cell / immunology*
  • Signal Transduction / immunology*


  • Adaptor Proteins, Signal Transducing
  • B cell linker protein
  • Carrier Proteins
  • Mitogens
  • Phosphoproteins
  • Receptors, Antigen, B-Cell
  • Protein-Tyrosine Kinases