期刊
MUCOSAL IMMUNOLOGY
卷 13, 期 4, 页码 626-636出版社
ELSEVIER SCIENCE INC
DOI: 10.1038/s41385-020-0266-x
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资金
- MSD Life Science Foundation
- Japan Society for the Promotion of Science (JSPS) Overseas Research Fellowships
- National Institutes of Health (NIH) [AI074878, AI095466, AI095608, AI102942]
- National Institutes of Allergy and Infectious Diseases (NIAID) [U19AI125378]
- German Research Foundation (DFG) [SFB 783]
- Burroughs Wellcome Fund
- Crohn's & Colitis Foundation
- Cure for IBD
- Rosanne H. Silberman Foundation
Thymic stromal lymphopoietin (TSLP) is a critical upstream cytokine inducing type 2 inflammation in various diseases, including asthma and atopic dermatitis. Accumulating evidence suggests that TSLP can directly stimulate a variety of immune cells, such as dendritic cells (DCs), basophils, T cells, and group 2 innate lymphoid cells (ILC2s). However, which cell types directly respond to TSLP in vivo and how TSLP initiates type 2 inflammation has remained controversial. To define the precise role of TSLP in vivo, for the first time we generated multiple cell lineage-specific TSLP receptor-deficient mice to systematically dissect the cell-intrinsic requirements for TSLP responsiveness in type 2 inflammation in the lung. In papain-induced innate immune-mediated type 2 airway inflammation, TSLP directly stimulated ILC2s, but not basophils, leading to enhanced type 2 inflammation. On the other hand, in OVA-induced adaptive immune-mediated type 2 airway inflammation, TSLP principally acted on DCs and CD4 + T cells during the sensitization phase, but not basophils or ILC2s, and facilitated the development of Th2 cell-mediated airway inflammation. Together, these findings reveal that TSLP activates distinct immune cell cascades in the context of innate and adaptive immune-mediated type 2 inflammation.
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