An epithelial Nfkb2 pathway exacerbates intestinal inflammation by supplementing latent RelA dimers to the canonical NF-κB module

Abstract excerpt

Significance The canonical NF-κB pathway mediates controlled nuclear activation of RelA factors, which induce proinflammatory genes. Uncontrolled RelA activity, however, fuels aberrant intestinal inflammation. What triggers pathological RelA activity in the colitogenic gut remains unclear. The noncanonical NF-κB module typically directs immune organogenesis involving Nfkb2 gene products. We find that this...

Topics

Share this publication in a Topic to start or enrich a Post.

• Share to Helicobacter pylori-related gastroenterology studies
• Share to Immune Response and Inflammation
• Share to NF-κB Signaling Pathways