| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 3294684 | Gastroenterology | 2013 | 21 Pages |
Abstract
PTPN22 expression is reduced in intestinal tissues of patients with active CD. PTPN22 regulates intracellular signaling events and is induced by IFN-γ in human monocytes. Knockdown of PTPN22 alters activation of inflammatory signal transducers, increasing secretion of T-helper 17-related inflammatory mediators. Genetic variants that reduce PTPN22 activity might contribute to the pathogenesis of CD by these mechanisms.
Keywords
MCP-1TGFICAM1MCP1IFN-γSOCS1IκBTh17SOCSIBDERKICAMNOD2T helperPTPN22Nucleotide-binding oligomerization domain-containing protein 2mRNAJnkJanus kinasec-Jun N-terminal kinaseMAPKmessenger RNASmall interfering RNAsiRNASTATinterferon γinterleukinCrohn's diseaseInflammatory bowel diseasetransforming growth factorT-betsuppressor of cytokine signalingSignal transducer and activator of transcriptioninhibitor of κBintracellular adhesion moleculemonocyte chemoattractant protein 1mitogen-activated protein kinaseJAKUlcerative colitisExtracellular signal–regulated kinase
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Authors
Marianne R. Spalinger, Silvia Lang, Achim Weber, Pascal Frei, Michael Fried, Gerhard Rogler, Michael Scharl,