ErbB4 signaling stimulates pro-inflammatory macrophage apoptosis and limits colonic inflammation.

ABSTRACT: Efficient clearance of pro-inflammatory macrophages from tissues after resolution of a challenge is critical to prevent prolonged inflammation. Defects in clearance can contribute to conditions such as inflammatory bowel disease, and thus may be therapeutically targetable. However, the signaling pathways that induce termination of pro-inflammatory macrophages are incompletely defined. We tested whether the ErbB4 receptor tyrosine kinase, previously not known to have role in macrophage biology, is involved in this process. In vitro, pro-inflammatory activation of cultured murine and human macrophages induced ErbB4 expression; in contrast, other ErbB family members were not induced in pro-inflammatory cells, and other innate immune lineages (dendritic cells, neutrophils) did not express dete

SUBMITTER: Schumacher MA 

PROVIDER: S-EPMC5386486 | biostudies-literature | 2017 Feb

REPOSITORIES: biostudies-literature