期刊
IMMUNITY
卷 50, 期 5, 页码 1289-+出版社
CELL PRESS
DOI: 10.1016/j.immuni.2019.04.006
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资金
- Swiss National Science Foundation, Switzerland [316030_150768, 310030_146130]
- European Community FP7 [602239 ATECT]
- University Research Priority Program (URPP) for Translational Cancer Research
- DOC fellowship from the Austrian Academy of Science
- DFG Cluster of Excellence Inflammation at Interfaces
- EU H2020 grant SYSCID [733100]
- DFG [CRC/TR 128]
- Hertie Stiftung, Germany
Pathogenic lymphocytes initiate the development of chronic inflammatory diseases. The cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) (encoded by Csf2) is a key communicator between pathogenic lymphocytes and tissue-invading inflammatory phagocytes. However, the molecular properties of GM-CSF-producing cells and the mode of Csf2 regulation in vivo remain unclear. To systematically study and manipulate GM-CSF+ cells and their progeny in vivo, we generated a fate-map and reporter of GM-CSF expression mouse strain (FROG). We mapped the phenotypic and functional profile of auto-aggressive T helper (Th) cells during neuroinflammation and identified the signature and pathogenic memory of a discrete encephalitogenic Th subset. These cells required interleukin-23 receptor (IL-23R) and IL-1R but not IL-6R signaling for their maintenance and pathogenicity. Specific ablation of this subset interrupted the inflammatory cascade, despite the unperturbed tissue accumulation of other Th subsets (e.g., Th1 and Th17), high-lighting that GM-CSF expression not only marks pathogenic Th cells, but that this subset mediates immunopathology and tissue destruction.
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