A myeloid-stromal niche and gp130 rescue in NOD2-driven Crohn's disease.

ABSTRACT: Crohn's disease is a chronic inflammatory intestinal disease that is frequently accompanied by aberrant healing and stricturing complications. Crosstalk between activated myeloid and stromal cells is critical in the pathogenicity of Crohn's disease^1,2, and increases in intravasating monocytes are correlated with a lack of response to anti-TNF treatment³. The risk alleles with the highest effect on Crohn's disease are loss-of-function mutations in NOD2^4,5, which increase the risk of stricturing⁶. However, the mechanisms that underlie pathogenicity driven by NOD2 mutations and the pathways that might rescue a lack of response to anti-TNF treatment remain largely uncharacterized. Here we use direct ex vivo analyses of patients who carry risk alleles

SUBMITTER: Nayar S 

PROVIDER: S-EPMC8284870 | biostudies-literature | 2021 May

REPOSITORIES: biostudies-literature