GITR‐GITRL interactions were found to enhance Th2 responses in helminthic infection and potentiated Th2 responses in a model of airway hyper‐responsiveness.26, 27 Following IL‐33 treatment, there was a significant reduction in expression of GITR on the ILC2 from PD‐1xRAG1−/− mice when compared with ILC2 from RAG1−/− mice (92 MFI ± 34 vs 131 MFI ± 21, respectively, P < .05 Mann Whitney test, Figure 5G,H). This evidence concerns the gene TNFRSF18 and helminthiasis.