The AMs and bone-marrow-derived macrophages isolated from CCR4-/- mice did not exhibit CCL17-dependent M1 activation but showed an M2 phenotype with higher expression of the nonsignaling CC chemokine scavenging receptor D6 in cell membranes [73], suggesting that scavenging receptor D6 acts as a novel component in regulating CCL17-mediated macrophage function and that CCL17-dependent activation of CCR4 in macrophages plays critical roles in the development of BLM-induced PF [73]. Here, CCR4 is linked to Bloom syndrome.