Journal
IMMUNITY
Volume 42, Issue 2, Pages 294-308Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2015.01.016
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Funding
- Global COE Program (Global Center for Education and Research in Immune System Regulation and Treatment)
- Ministry of Education, Culture, Sports, Science, and Technology of Japan [26221305, 21390147, 24592083, 24790461, 25860352, 25893032]
- Ministry of Health, Labor, and Welfare
- Astellas Foundation for Research on Metabolic Disorders
- Uehara Memorial Foundation
- Kanae Foundation for the Promotion of Medical Science
- Princes Takamatsu Cancer Research Fund
- Takeda Science Foundation
- Japanese Society for the Promotion of Science postdoctoral fellowship [2109747]
- Grants-in-Aid for Scientific Research [21390147, 24592083, 25860352, 24790461, 26221305, 24591475, 26870172, 25893032] Funding Source: KAKEN
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Memory CD4(+) T helper (Th) cells provide long-term protection against pathogens and are essential for the development of vaccines; however, some antigen-specific memory Th cells also drive immunerelated pathology, including asthma. The mechanisms regulating the pathogenicity of memory Th cells remain poorly understood. We found that interleukin-33 (IL-33)-ST2 signals selectively licensed memory Th2 cells to induce allergic airway inflammation via production of IL-5 and that the p38 MAP kinase pathway was a central downstream target of IL-33-ST2 in memory Th2 cells. In addition, we found that IL-33 induced upregulation of IL-5 by memory CD4(+) T cells isolated from nasal polyps of patients with eosinophilic chronic rhinosinusitis. Thus, IL-33ST2-p38 signaling appears to directly instruct pathogenic memory Th2 cells to produce IL-5 and induce eosinophilic inflammation.
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