Cd177, a glycosylphosphatidylinositol (GPI)-anchored protein, is specifically expressed in neutrophils. It is involved in various functions such as neutrophil migration, as it associates with β2 integrins and recognizes platelet endothelial cell adhesion molecule 1 (PECAM-1) [2]. It also mediates the surface expression of the antineutrophil cytoplasmic antibody antigen proteinase 3 [2]. Cd177-related pathways may be crucial for maintaining immune homeostasis and host defense mechanisms. Genetic models, like gene knockout mouse models, are valuable for studying its functions.

In the context of Inflammatory Bowel Disease (IBD), Cd177 -/- mice developed more severe colitis upon dextran sulfate sodium (DSS) insults compared to wild-type mice. This indicates that CD177+ neutrophils play a protective role in IBD through increased bactericidal activity and IL-22 production [1].

In biliary atresia, Cd177 -/- BALB/c mice exhibited delayed disease onset and reduced morbidity and mortality, suggesting that CD177+ cells play an important role in the initiation of BA pathogenesis via NET formation [3].

In the gut, depletion of CD177+ neutrophils in mice caused expansion of colitogenic TCRγδ+CD8αα+ intraepithelial lymphocytes (IELs), increased intestinal inflammation, and dysbiosis. This shows that neutrophils, especially the CD177+ subset, inhibit intestinal inflammation by promoting microbiota-derived dimethyl fumarate (DMF) to regulate TCRγδ+CD8αα+ IEL activation [4].

In conclusion, Cd177 is essential for neutrophil-mediated functions in various disease conditions. Gene knockout mouse models have revealed its role in protecting against IBD, contributing to the pathogenesis of biliary atresia, and maintaining intestinal homeostasis. Understanding Cd177's functions provides insights into the underlying mechanisms of these diseases, potentially leading to the development of novel therapeutic strategies.