Abstract
The best studied mechanisms of B cell tolerance are receptor editing, clonal deletion and anergy. All of these mechanisms of B cell tolerance depend on the induction of signaling downstream of the B cell receptor by self-antigens. Another important and distinct mechanism of B cell tolerance involves the repression of antigen receptor signaling rather than its induction, utilizes the Lyn Src-family kinase, the SHP-1 tyrosine phosphatase, inhibitory members of the Siglec family, and a carbohydrate-modifying enzyme that is capable of negatively regulating B cell receptor activation known as sialic acid acetylesterase.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Acetylesterase
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Animals
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Autoantigens / immunology
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Autoimmune Diseases / enzymology*
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B-Lymphocytes / enzymology
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B-Lymphocytes / immunology*
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Carbohydrate Metabolism
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Carboxylic Ester Hydrolases / metabolism*
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Clonal Deletion
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Down-Regulation
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Humans
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Immune Tolerance*
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Lymphocyte Activation
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Mice
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N-Acetylneuraminic Acid / metabolism
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Protein Tyrosine Phosphatase, Non-Receptor Type 6 / metabolism
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Receptors, Interleukin-4 / metabolism
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src-Family Kinases / metabolism
Substances
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Autoantigens
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Receptors, Interleukin-4
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src-Family Kinases
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Carboxylic Ester Hydrolases
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Acetylesterase
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sialate O-acetylesterase
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Protein Tyrosine Phosphatase, Non-Receptor Type 6
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N-Acetylneuraminic Acid