This is consistent with previous findings that show in vivo C5aR targeting during initial allergen exposure can either induce or enhance Th2 adaptive immunity [52] and a knockout asthma mouse model C5aR (−/−) exhibits excessive IL17A production that drives a severe asthma phenotype by enhancing Th2 cell-driven pathology [53], [54]. The gene discussed is C5AR1; the disease is asthma.