Open AccessThe role for protein tyrosine phosphatase non‐receptor type 22 in regulating intestinal homeostasis
Author(s) -
Spalinger Marianne R,
Scharl Michael
Publication year - 2016
Publication title -
ueg journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.667
H-Index - 35
eISSN - 2050-6414
pISSN - 2050-6406
DOI - 10.1177/2050640615600115
Subject(s) - ptpn22 , inflammatory bowel disease , medicine , immunology , immune system , myeloid , protein tyrosine phosphatase , inflammation , homeostasis , microbiology and biotechnology , disease , biology , receptor , gene , genetics , genotype , single nucleotide polymorphism
Inflammatory bowel disease represents a chronic intestinal inflammation. Recent knowledge suggests a crucial role for genetic, immunological and bacterial factors in inflammatory bowel disease pathogenesis. Variations within the gene locus encoding PTPN22 have been associated with inflammatory bowel disease. PTPN22 is critically involved in controlling immune cell activation and thereby plays an important role in maintaining intestinal homeostasis. Although in B and T cells the mechanism showing how PTPN22 affects cell signalling pathways is well studied, its role in myeloid cells remains less defined. Regulation of the innate immune system plays an essential role in the intestine, and levels of PTPN22 in myeloid cells are drastically reduced in the intestine of inflammatory bowel disease patients. Therefore, additional studies to define the role of PTPN22 in myeloid cells might clearly enhance our understanding of how PTPN22 contributes to intestinal homeostasis.