Following infection with N. brasiliensis, Nmu expression was increased in both the lung and the gut, resulting in robust ILC2 responses through Nmur1 and worm clearance (Figure 2D); in contrast, if adoptively transferred into Rag2 Il2rg deficient mice, Nmur1 (NMU receptor 1) deficient ILC2s produce significantly reduced amounts of type-2 cytokine than their gene sufficient counterparts (79, 80). Here, NMUR1 is linked to infection.