Ccr3, also known as CD193, is a G-protein coupled receptor (GPCR) [2,4,6,7]. It plays a crucial role in inflammatory, autoimmune, and neuronal migration mechanisms [1]. Ccr3 is associated with the recruitment of leukocyte subsets in atopic diseases, as ligands like RANTES, MCP-3, MCP-4, and eotaxins bind to it, leading to eosinophil chemotaxis and other pro-inflammatory activities [2,4]. It is also expressed on various cell types including eosinophils, basophils, mast cell subpopulations, activated Th2 cells, macrophages, and airway epithelial cells, thus being closely related to asthma and allergic diseases [6].

In male mice lacking Ccr3, there is a cortical bone phenotype with thin femoral cortical bone, reduced cortical bone volume and thickness, and increased periosteal mineralization. This phenotype is not present in female mice, indicating that Ccr3's role in cortical bone turnover may be related to sex hormones [3]. In carcinoma cell lines, blocking Ccr3 induces polyploidization associated with epithelial-mesenchymal transition (EMT) processes via the PI3K/Akt/GSK-3β signaling pathway, and the converted cells show enhanced mobile and proliferation abilities [5].

In summary, Ccr3 is a key receptor involved in inflammation, especially in allergic-related diseases. Gene-knockout mouse models have revealed its sex-specific role in cortical bone development and its influence on cancer-related cell behaviors such as EMT. Understanding Ccr3's functions can provide potential therapeutic targets for diseases like asthma, allergic diseases, and potentially for bone-related and cancer-related conditions.