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. Author manuscript; available in PMC: 2014 Dec 1.
Published in final edited form as: Curr Opin Immunol. 2013 Aug 31;25(6):738–744. doi: 10.1016/j.coi.2013.07.013

Figure 1. ILC2s influence the development of Th2 cytokine-mediated inflammation through multiple pathways.

Figure 1

In response to helminth parasites or allergens, epithelial cells, macrophages, and mast cells at multiple barrier surfaces, including the gut, lung and skin, produce the cytokines IL-25, IL-33 and TSLP or eicosanoids that regulate the accumulation and activation of ILC2s. Activated ILC2s produce effector molecules such as amphiregulin (Areg), IL-4, IL-5, IL-9 and IL-13. These factors influence the responses and cytokine production of innate effector cells, including alternatively activated macrophages (AAMØ), eosinophils, mast cells and basophils. In addition, ILC2s influence adaptive responses through production of effector molecules, and potentially interact with B cells and T cells through expression of ICOS or MHC II, respectively. Together, ILC2-derived effector molecules and the influence of ILC2s on other innate and adaptive immune cells contribute to the development of type 2 cytokine-mediated inflammation in the gut, lung and skin.