Research ArticleMACROPHAGES

IRF5 guides monocytes toward an inflammatory CD11c+ macrophage phenotype and promotes intestinal inflammation

See allHide authors and affiliations

Science Immunology  22 May 2020:
Vol. 5, Issue 47, eaax6085
DOI: 10.1126/sciimmunol.aax6085

You are currently viewing the editor's summary.

View Full Text

Log in to view the full text

Log in through your institution

Log in through your institution

Targeting overzealous macrophages

Intestinal homeostasis relies on maintenance of a complex set of interactions between intestinal microbiota and the intestinal immune system. Pathogens that colonize the gut invariably disrupt these interactions and promote intestinal inflammation. Here, Corbin et al. have used a mouse pathobiont, Helicobacter hepaticus, that causes inflammation akin to human inflammatory bowel disease (IBD) to study the role of intestinal macrophages in driving inflammation. Using this model, they found the transcription factor IRF5 to be a critical regulator of macrophage inflammatory potential and that deletion of IRF5 rendered mice resistant to H. hepaticus–driven intestinal inflammation. Their studies propose IRF5 and molecules upstream of IRF5 to be potential drug targets in the treatment of human IBD.

View Full Text

Stay Connected to Science Immunology