Cathelicidins use human formyl peptide receptor-like-1 (FPRL1) to induce neutrophil and monocyte migration (112, 114) or activate plasmacytoid and myeloid DCs via TLR7, 8 or 9, all of which have been shown to contribute to autoimmune disease and wound healing (197–200). This evidence concerns the gene FPR2 and autoimmune disease.