Academic Journal

Epithelial Cell-derived IL-25, but not Th17 cell-derived IL-17 or IL-17F, is Crucial for Murine Asthma1

Bibliographic Details
Title: Epithelial Cell-derived IL-25, but not Th17 cell-derived IL-17 or IL-17F, is Crucial for Murine Asthma1
Authors: Suzukawa, Maho, Morita, Hideaki, Nambu, Aya, Arae, Ken, Shimura, Eri, Shibui, Akiko, Yamaguchi, Sachiko, Suzukawa, Keigo, Nakanishi, Wakako, Oboki, Keisuke, Kajiwara, Naoki, Ohno, Tatsukuni, Ishii, Akina, Körner, Heinrich, Cua, Daniel J, Suto, Hajime, Yoshimoto, Takayuki, Iwakura, Yoichiro, Yamasoba, Tatsuya, Ohta, Ken, Sudo, Katsuko, Saito, Hirohisa, Okumura, Ko, Broide, David, Matsumoto, Kenji, Nakae, Susumu
Publication Year: 2012
Collection: PubMed Central (PMC)
Subject Terms: Article
Description: IL-17A, IL-17F and IL-25 are ligands for IL-17RA. In the present study, we demonstrated that IL-25-deficient mice, but not IL-17A-, IL-17F-, IL-17A/F-, IL-23p19- and ROR-γt-deficient mice, showed significant suppression of the number of eosinophils and the levels of proinflammatory mediators in bronchoalveolar lavage fluids, airway hyperresponsiveness to methacholine, or ovalbumin-specific IgG1 and IgE levels in the serum during ovalbumin-induced Th2-type/eosinophilic airway inflammation, without any effect on lung DC migration or antigen-specific memory-Th2-cell expansion during antigen sensitization. By adoptive transfer of either T cells, mast cells or bone marrow cells from IL-25-deficient mice, we found that IL-25 produced by airway structural cells such as epithelial cells—but not by such hematopoietic stem-cell-origin immune cells as T cells and mast cells—was indispensable for induction of Th2-type/eosinophilic airway inflammation by activating lung epithelial cells and eosinophils. Therefore, airway structural-cell-derived IL-25—rather than Th17-cell-derived IL-17A and IL-17F—is responsible for induction of local inflammation by promoting activation of lung epithelial cells and eosinophils in the elicitation phase—but is not required for antigen-specific Th2 cell differentiation in the sensitization phase—of Th2-type/eosinophilic airway inflammation.
Document Type: text
Language: English
Relation: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3812057; http://www.ncbi.nlm.nih.gov/pubmed/22942422; http://dx.doi.org/10.4049/jimmunol.1200461
DOI: 10.4049/jimmunol.1200461
Availability: https://doi.org/10.4049/jimmunol.1200461
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3812057
http://www.ncbi.nlm.nih.gov/pubmed/22942422
Accession Number: edsbas.CECEF65F
Database: BASE
Description
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