CCR3 is a G protein-coupled chemokine receptor primarily functioning as a CC chemokine receptor expressed on immune effector cells. Structurally, CCR3 mediates its effects through phospholipase C activation and G protein coupling 1, localizing to the plasma membrane and participating in heterotrimeric G protein-mediated signaling. Mechanistically, CCR3 binds CC chemokines including eotaxin, which stimulates eosinophil migration from blood vessels into tissues via the chemotaxis pathway 2. The receptor is preferentially expressed on Th2 cells, mast cells, and eosinophils 1, and can function as an alternative HIV-1 co-receptor with CD4 3. Disease relevance is substantial: CCR3 expression correlates with allergic diseases including asthma, atopic dermatitis, and allergic rhinitis through eosinophil recruitment 1. CCR3 also marks vascularized corneal tissue in neovascularization 4 and appears on tumor cells in CD30+ lymphoproliferative disorders 5. Clinically, CCR3 antagonism represents a therapeutic strategy—antisense inhibition of CCR3 reduced allergen-induced eosinophilic responses and early asthmatic reactions by 46% 6, while simvastatin suppressed IL-5-induced CCR3 expression and eosinophilic infiltration in allergic rhinitis models 7. Small molecule CCR3 antagonists are under development as orally bioavailable treatments for allergic diseases.