CCL17 is a C-C chemokine that recruits T lymphocytes, particularly Th2 cells, through binding to CCR4 on the T-cell surface, playing a central role in type 2 inflammatory and immunological responses. Beyond its classical chemotactic function, CCL17 mediates GM-CSF-driven pain and inflammation, maintains microglial morphology in the brain, and promotes wound healing through fibroblast migration. In disease contexts, CCL17 contributes to myocardial injury after infarction by suppressing regulatory T cell recruitment through biased CCR4 signaling 1, and elevated CCL17 associates with invasive pituitary adenoma through lactate-induced M2 macrophage polarization 2. CCL17 is a biomarker of type 2 inflammation in atopic dermatitis and allergic asthma, with dupilumab and lebrikizumab—which target IL-13 signaling upstream of CCL17 expression—achieving 72–83% reductions in serum CCL17 in pediatric atopic dermatitis and significant decreases in asthma biomarkers, respectively 34. Genetic polymorphisms in CCL17 associate with atopic dermatitis and Kawasaki disease susceptibility 56. CCL17 represents a therapeutic target in type 2 inflammatory diseases and a clinical biomarker of disease activity and prognosis.