Human C-C Chemokine Receptor Type 3 (CCR3) Protein

Background

C-C Chemokine Receptor Type 3 (CCR3) is a G-protein-coupled receptor (GPCR) that binds multiple chemokines, including CCL11 (eotaxin), CCL24 (eotaxin-2), and CCL5 (RANTES). CCR3 is predominantly expressed on eosinophils, basophils, mast cells, and Th2 lymphocytes, making it a critical regulator of allergic inflammation and immune responses. CCR3 signaling promotes eosinophil chemotaxis, activation, and survival, leading to the accumulation of eosinophils at sites of allergic inflammation, such as in asthma, allergic rhinitis, and atopic dermatitis. Additionally, CCR3 expression on retinal pigment epithelial cells and microglia links it to age-related macular degeneration (AMD) and other neuroinflammatory conditions. In parasitic infections, CCR3 plays a protective role by guiding eosinophils to sites of helminth invasion, contributing to parasite clearance. However, excessive CCR3 activation in chronic inflammation can exacerbate tissue damage and fibrosis. CCR3 is also expressed in certain cancers and may promote angiogenesis and tumor progression by recruiting pro-inflammatory cells to the tumor microenvironment. As a key mediator of allergic and inflammatory diseases, CCR3 is a promising target for therapeutic intervention. CCR3 antagonists and neutralizing antibodies are being explored for treating eosinophilic disorders, asthma, and ocular diseases, where inhibition of CCR3 can reduce eosinophil recruitment, inflammation, and tissue damage. Ongoing research into CCR3 biology continues to uncover its broader implications in inflammation, immunity, and cancer.