期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 217, 期 9, 页码 -出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20190865
关键词
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资金
- National Institutes of Health [R01 AI040618, T32 HL116275, K08 HL140173, P30 DK040561]
- National Institutes of Health Shared Instrumentation program [1S10OD012027-01A1, 1S10OD016372-01, 1S10RR020936-01, 1S10RR023440-01A1]
Memory CD4(+) T helper type 2 (Th2) cells drive allergic asthma, yet the mechanisms whereby tissue-resident memory Th2 (Th2 Trm) cells and circulating memory Th2 cells collaborate in vivo remain unclear. Using a house dust mite (HDM) model of allergic asthma and parabiosis, we demonstrate that Th2 Trm cells and circulating memory Th2 cells perform nonredundant functions. Upon HDM rechallenge, circulating memory Th2 cells trafficked into the lung parenchyma and ignited perivascular inflammation to promote eosinophil and CDC+ T cell recruitment. In contrast, Th2 Trm cells proliferated near airways and induced mucus metaplasia, airway hyperresponsiveness, and airway eosinophil activation. Transcriptional analysis revealed that Th2 Trm cells and circulating memory Th2 cells share a core Th2 gene signature but also exhibit distinct transcriptional profiles. Th2 Trm cells express a tissue-adaptation signature, including genes involved in regulating and interacting with extracellular matrix. Our findings demonstrate that Th2 Trm cells and circulating memory Th2 cells are functionally and transcriptionally distinct subsets with unique roles in promoting allergic airway disease.
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