 IL8, IL13, IL12, and IL5) by neutrophils, eosinophils, monocytes, Innate lymphoid cells, and/or macrophages, as well as suppress proliferation and production of IgM and IgG antibodies by B lymphocytes.These actions appear to involve stimulating anti-inflammatory signaling pathways, but also blocking the actions of other ALX/FPR ligands which simulate pro-inflammatory pathways.Transgenic mice made to overexpress ALX/FPR exhibit markedly reduced inflammatory responses to diverse insults.