The encephalitogenicity of TH17 cells is dependent on IL-1- and IL-23-induced production of the cytokine GM-CSF
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Title
The encephalitogenicity of TH17 cells is dependent on IL-1- and IL-23-induced production of the cytokine GM-CSF
Authors
Keywords
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Journal
NATURE IMMUNOLOGY
Volume 12, Issue 6, Pages 568-575
Publisher
Springer Nature
Online
2011-04-25
DOI
10.1038/ni.2031
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- Cutting Edge: NKT Cells Constitutively Express IL-23 Receptor and ROR t and Rapidly Produce IL-17 upon Receptor Ligation in an IL-6-Independent Fashion
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- Fate mapping of IL-17-producing T cells in inflammatory responses
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- IL-23 Drives Pathogenic IL-17-Producing CD8+ T Cells
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- C-C chemokine receptor 6–regulated entry of TH-17 cells into the CNS through the choroid plexus is required for the initiation of EAE
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- The interleukin 23 receptor is essential for the terminal differentiation of interleukin 17–producing effector T helper cells in vivo
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- IL-9 induces differentiation of TH17 cells and enhances function of FoxP3+ natural regulatory T cells
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- IL‐21 and IL‐21R are not required for development of Th17 cells and autoimmunityin vivo
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- RORγ-Expressing Th17 Cells Induce Murine Chronic Intestinal Inflammation via Redundant Effects of IL-17A and IL-17F
- (2008) Moritz Leppkes et al. GASTROENTEROLOGY
- T Helper 17 Lineage Differentiation Is Programmed by Orphan Nuclear Receptors RORα and RORγ
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- GM-CSF mediates autoimmunity by enhancing IL-6–dependent Th17 cell development and survival
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- Regulation of inflammatory responses by IL-17F
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