Abstract
Mice in which the Lyn, Cd22, or Shp-1 gene has been disrupted have hyperactive B cells and autoantibodies. We find that in the absence of Lyn, the ability of CD22 to become tyrosine phosphorylated after ligation of mIg, to recruit SHP-1, and to suppress mIg-induced elevation of intracellular [Ca2+] is lost. Therefore, Lyn is required for the SHP-1-mediated B cell suppressive function of CD22, accounting for similarities in the phenotypes of these mice.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Amino Acid Sequence
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Animals
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Antigens, CD / physiology*
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Antigens, Differentiation, B-Lymphocyte / physiology*
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Autoimmunity*
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B-Lymphocytes / physiology*
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Calcium / physiology
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Cell Adhesion Molecules*
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Immune Tolerance
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Intracellular Signaling Peptides and Proteins
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Lectins*
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Mice
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Mice, Knockout
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Phosphorylation
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Phosphotyrosine / metabolism
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Protein Tyrosine Phosphatase, Non-Receptor Type 11
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Protein Tyrosine Phosphatase, Non-Receptor Type 6
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Protein Tyrosine Phosphatases / physiology*
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Receptors, Antigen, B-Cell / physiology*
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Sialic Acid Binding Ig-like Lectin 2
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Signal Transduction
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Spleen / cytology
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src-Family Kinases / physiology*
Substances
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Antigens, CD
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Antigens, Differentiation, B-Lymphocyte
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Cd22 protein, mouse
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Cell Adhesion Molecules
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Intracellular Signaling Peptides and Proteins
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Lectins
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Receptors, Antigen, B-Cell
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Sialic Acid Binding Ig-like Lectin 2
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Phosphotyrosine
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lyn protein-tyrosine kinase
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src-Family Kinases
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Protein Tyrosine Phosphatase, Non-Receptor Type 11
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Protein Tyrosine Phosphatase, Non-Receptor Type 6
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Protein Tyrosine Phosphatases
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Ptpn11 protein, mouse
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Ptpn6 protein, mouse
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Calcium