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- W2725687573 endingPage "330" @default.
- W2725687573 startingPage "330" @default.
- W2725687573 abstract "An allelic variant of the protein tyrosin phosphatase non-receptor 22 (PTPN22) gene, PTPN22 R620W, constitutes the strongest non-HLA genetic risk factor for the development of type 1 diabetes (T1D). A number of studies using mouse models have addressed how PTPN22 predisposes to T1D. PTPN22 downmodulation, overexpression or expression of the variant gene in genetically manipulated mice has generated controversial results. These discrepancies probably derive from the fact that PTPN22 has differential effects on innate and adaptive immune responses. Moreover, the effects of PTPN22 are dependent on other genetic variables. Here we discuss these findings and try to explain the discrepancies. Exploring the mechanism by which PTPN22 contributes to islet-specific autoimmunity could help us understand its role in T1D pathogenesis and exploit it as a potential therapeutic target to prevent the disease." @default.
- W2725687573 created "2017-07-14" @default.
- W2725687573 creator A5042278832 @default.
- W2725687573 creator A5070810958 @default.
- W2725687573 date "2017-01-01" @default.
- W2725687573 modified "2023-09-27" @default.
- W2725687573 title "PTPN22 and islet-specific autoimmunity: What have the mouse models taught us?" @default.
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- W2725687573 doi "https://doi.org/10.4239/wjd.v8.i7.330" @default.
- W2725687573 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5507829" @default.
- W2725687573 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/28751955" @default.
- W2725687573 hasPublicationYear "2017" @default.
- W2725687573 type Work @default.