Abstract
The discovery that a single amino acid substitution in the PTPN22 protein tyrosine phosphatase can predispose to so many autoimmune diseases (see chapters 2 and 3), even when present in a single copy, raises many questions regarding the broader significance of this observation. Is there something unique about PTPN22 or are genetic variants of other protein tyrosine phosphatases likely also associated with autoimmune disease? If so, will polymorphisms in other phosphatases be found in the same spectrum of diseases? Are protein tyrosine phosphatases like PTPN22 good drug targets for the treatment of human autoimmunity? In this review, I offer some basis for thinking about these questions.
Publication types
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Research Support, N.I.H., Extramural
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Review
MeSH terms
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Animals
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Autoimmune Diseases / drug therapy
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Autoimmune Diseases / enzymology*
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Autoimmune Diseases / genetics
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Autoimmune Diseases / immunology
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Autoimmunity / genetics*
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Autoimmunity / immunology
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Humans
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Leukocyte Common Antigens / genetics
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Leukocyte Common Antigens / metabolism
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Polymorphism, Genetic
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Protein Tyrosine Phosphatase, Non-Receptor Type 22
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Protein Tyrosine Phosphatases / antagonists & inhibitors
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Protein Tyrosine Phosphatases / genetics
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Protein Tyrosine Phosphatases / metabolism*
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T-Lymphocytes / immunology
Substances
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Leukocyte Common Antigens
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PTPN22 protein, human
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PTPRC protein, human
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Protein Tyrosine Phosphatase, Non-Receptor Type 22
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Protein Tyrosine Phosphatases