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Ferred resistance against the infection and promoted a Th2 response (IL-4, IL-13 and IL-9) whereas it suppressed Th1- and Th17-type cytokine expression (IFN, TNF and IL-6).209 In the context of systemic inflammation, such as that occurring during sepsis, IL-33 was found to be beneficial.210 Indeed, in the murine CLP model, extracellular IL-33 inhibited the expression of G protein-coupled receptor

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