pubmed-article:20204370 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:20204370 | lifeskim:mentions | umls-concept:C0085536 | lld:lifeskim |
pubmed-article:20204370 | lifeskim:mentions | umls-concept:C0004368 | lld:lifeskim |
pubmed-article:20204370 | lifeskim:mentions | umls-concept:C1518071 | lld:lifeskim |
pubmed-article:20204370 | lifeskim:mentions | umls-concept:C0020124 | lld:lifeskim |
pubmed-article:20204370 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:20204370 | pubmed:dateCreated | 2010-5-11 | lld:pubmed |
pubmed-article:20204370 | pubmed:abstractText | A relatively large number of protein tyrosine phosphatases (PTPs) are known to regulate signaling through the T cell receptor (TCR). Recent human genetics studies have shown that several of these PTPs are encoded by major autoimmunity genes. Here, we will focus on the lymphoid tyrosine phosphatase (LYP), a critical negative modulator of TCR signaling encoded by the PTPN22 gene. The functional analysis of autoimmune-associated PTPN22 genetic variants suggests that genetic variability of TCR signal transduction contributes to the pathogenesis of autoimmunity in humans. | lld:pubmed |
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