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PTPN22 and islet-specific autoimmunity: What have the mouse models taught us?

Authors
  • Galvani, Giuseppe1
  • Fousteri, Georgia1
  • 1 Giuseppe Galvani, Georgia Fousteri, Diabetes Research Institute, IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy. , (Georgia)
Type
Published Article
Journal
World Journal of Diabetes
Publisher
Baishideng Publishing Group Co (World Journal of Diabetes)
Publication Date
Jul 15, 2017
Volume
8
Issue
7
Pages
330–336
Identifiers
DOI: 10.4239/wjd.v8.i7.330
PMID: 28751955
Source
Medline
Keywords
License
Unknown

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.

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