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Abstract
Inflammatory bowel disease is a complex multifactorial disease with a strong genetic component. Recent studies have identified innate immunity (NOD2), autophagy (ATG16L1) and Th17 pathway (IL23R) genes in the pathogenesis of Crohn’s disease. The pathogenesis of ulcerative colitis (UC) is less clear; however, there is growing evidence that proteins involved in the apical junction complex are involved in UC. Here we review the up-to-date studies on the genetic basis for IBD and explore the newly described UC-associated apical junction complex pointing to a primary defect in barrier defense. We will focus on the PTPRS (encoding PTPσ) gene and discuss its and other apical junction complex proteins’ role in the pathogenesis of UC.
Financial & competing interests disclosure
Work from the authors’ laboratory was supported by the Canadian Institute of Health Research (CIHR) to Daniela Rotin, the Crohn’s Colitis Foundation of Canada (CCFC) to Daniela Rotin and a Thrasher Research Fund New Investigators Grant to Aleixo M Muise. Aleixo M Muise is supported by a fellowship from the Canadian Child Health Clinician Scientist Program (Strategic Training Initiatives in Health Research Program – CIHR). Daniela Rotin holds a Canada Research Chair (Tier I) from the Canada Foundation for Innovation/CIHR.
The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.
