Journal article
CCR2 defines in vivo development and homing of IL-23-driven GM-CSF-producing Th17 cells
EE Kara, DR McKenzie, CR Bastow, CE Gregor, KA Fenix, AD Ogunniyi, JC Paton, M Mack, DR Pombal, C Seillet, B Dubois, A Liston, KPA Macdonald, GT Belz, MJ Smyth, GR Hill, I Comerford, SR McColl
Nature Communications | Published : 2015
DOI: 10.1038/ncomms9644
Abstract
IL-17-producing helper T (Th17) cells are critical for host defense against extracellular pathogens but also drive numerous autoimmune diseases. Th17 cells that differ in their inflammatory potential have been described including IL-10-producing Th17 cells that are weak inducers of inflammation and highly inflammatory, IL-23-driven, GM-CSF/IFN 3-producing Th17 cells. However, their distinct developmental requirements, functions and trafficking mechanisms in vivo remain poorly understood. Here we identify a temporally regulated IL-23-dependent switch from CCR6 to CCR2 usage by developing Th17 cells that is critical for pathogenic Th17 cell-driven inflammation in experimental autoimmune enceph..
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Awarded by National Science Foundation
Funding Acknowledgements
We thank Professor Tracey Handel (University of California, La Jolla, USA) and the late Professor Ian Clark Lewis for recombinant chemokines and chemokine receptor antagonists; Dr Josef Ngyuen (Royal Adelaide Hospital, Adelaide, Australia) for mouse irradiation; Professor Brigitta Stockinger (Medical Research Council National Institute for Medical Research, UK) for B6.1117ac"Rosa26'YFP mice; Dr Christian Engwerda (QIMR Berghofer Medical Research Institute, Australia) for B6.Ccr2 - mice; Professor Bernhard Baune (University of Adelaide, Australia) for B6. Tnf- I, B6. Tnfrsfl a- I and B6. Tnfrsflb I - mice; Professor Carola Vinuesa (John Curtin School of Medical Research, Australia) for B6. Tcra- I - mice; Staff of the Laboratory Animal Services of the University of Adelaide for Animal Husbandry; and Staff of the Detmold Facility (IMVS, Australia) for some cell sorting experiments. This work was supported by funding held by S.R.M. and IC. from National Health and Medical Research Council (NH&MRC) Grant 1066781. IC. is supported by funds from Multiple Sclerosis Research Australia. M.J.S. is supported by an NH&MRC Research Fellowship (1078671). E.E.K. is supported by an Australian Postgraduate Award and the Norman and Patricia Polglase Scholarship.