Journal article
Interleukin-33 Induces the Enzyme Tryptophan Hydroxylase 1 to Promote Inflammatory Group 2 Innate Lymphoid Cell-Mediated Immunity
AL Flamar, CSN Klose, JB Moeller, T Mahlakõiv, NJ Bessman, W Zhang, S Moriyama, V Stokic-Trtica, LC Rankin, GG Putzel, HR Rodewald, Z He, L Chen, SA Lira, G Karsenty, D Artis
Immunity | CELL PRESS | Published : 2020
Abstract
IL-33 is a potent activator of type 2 immune responses via the stimulation of ILC2s, but the downstream pathways triggered in these cells are poorly defined. Flamar and colleagues show that IL-33 controls tryptophan hydroxylase 1 expression in ILC2s, which is required for type 2 immunity against worm infections.
Grants
Awarded by National Institutes of Health
Funding Acknowledgements
We thank the members of the Artis lab for critically reading the manuscript and the epigenomics core at Weill Cornell Medicine for carrying out the RNA sequencing. The work was supported by grants from the German Research Foundation (DFG; KL 2963/1-1 and KL 2963/2-1 to C.S.N.K. and SFB 873-B11 to H.-R.R.), the European Research Council (Starting Grant 803087 to C.S.N.K. and Advanced Grant 742883 to H.-R.R.), the Novo Nordic Foundation (14052 to J.B.M.), a National Institutes of Health (NIH) fellowship (F32AI124517 to N.J.B), JSPS Overseas Research Fellowships (to S.M.), the NIH (AI074878, AI095466, AI095608, and AI102942 to D.A. and 2P01AG032959-09 to G.K.), the Burroughs Wellcome Fund (to D.A.), the Crohn's and Colitis Foundation of America (to T.M. and D.A.), Cure for IBD (to D.A.), and the Rosanne H. Silberman Foundation (to D.A.).