An IFN-STAT Axis Augments Tissue Damage and Inflammation in a Mouse Model of Crohn's Disease.

ABSTRACT: Blocking interferon-function by therapeutic intervention of the JAK-STAT-axis is a novel promising treatment option for inflammatory bowel disease (IBD). Although JAK inhibitors have proven efficacy in patients with active ulcerative colitis (UC), they failed to induce clinical remission in patients with Crohn's disease (CD). This finding strongly implicates a differential contribution of JAK signaling in both entities. Here, we dissected the contribution of different STAT members downstream of JAK to inflammation and barrier dysfunction in a mouse model of Crohn's disease like ileitis and colitis (Casp8 ^ΔIEC mice). Deletion of STAT1 in Casp8 ^ΔIEC mice was associated with reduced cell death and a partial rescue of Paneth cell function in th

SUBMITTER: Stolzer I 

PROVIDER: S-EPMC8205542 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature