Intestinal epithelial PTPN2 limits pathobiont colonization by immune-directed antimicrobial responses.

ABSTRACT: Loss of activity of the inflammatory bowel disease (IBD) susceptibility gene, protein tyrosine phosphatase non-receptor type 2 (PTPN2), is associated with altered microbiome composition in both human subjects and mice. Furthermore, expansion of the bacterial pathobiont, adherent-invasive E. coli (AIEC), is strongly linked to IBD pathogenesis. The mechanism by which intestinal epithelial cells (IEC) maintain equilibrium between commensal microbiota and immune cells to restrict invading pathobionts is poorly understood. Here, we investigated the role of IEC-specific PTPN2 in regulating AIEC colonization. Tamoxifen-inducible, intestinal epithelial cell-specific Ptpn2 knockout mice (Ptpn2^∆IEC) and control Ptpn2^fl/fl mice were infected wi

SUBMITTER: Chatterjee P 

PROVIDER: S-EPMC12445515 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature