TWEAK/Fn14 Is Overexpressed in Crohn's Disease and Mediates Experimental Ileitis by Regulating Critical Innate and Adaptive Immune Pathways.

ABSTRACT:

Background & aims

Crohn's disease (CD) is a debilitating inflammatory disorder that affects more than 1.6 million people in North America alone. Members of the tumor necrosis factor superfamily are key regulators of intestinal inflammation; specifically, tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor, fibroblast growth factor-inducible 14 (Fn14), are involved in normal and pathologic tissue remodeling. Our aim was to determine the role of TWEAK/Fn14 in CD and a murine model of CD-like ileitis (ie, SAMP1/YitFc [SAMP] strain).

Methods

SAMP mice deficient in Fn14 (SAMP × Fn14^-/-) were developed and a detailed time-course study was performed evaluating ileal tissues by histology and stereomicroscopy, as well as quantitative polymerase ch

SUBMITTER: Di Martino L 

PROVIDER: S-EPMC6718944 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature