دورية أكاديمية
أعرض في EDS

TL1A priming induces a multi-cytokine Th9 cell phenotype that promotes robust allergic inflammation in murine models of asthma.

التفاصيل البيبلوغرافية
العنوان: TL1A priming induces a multi-cytokine Th9 cell phenotype that promotes robust allergic inflammation in murine models of asthma.
المؤلفون: Niese ML; Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN, USA., Pajulas AL; Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN, USA., Rostron CR; Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN, USA., Cheung CCL; Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN, USA., Krishnan MS; Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN, USA., Zhang J; Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN, USA., Cannon AM; Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN, USA., Kaplan MH; Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN, USA. Electronic address: mkaplan2@iupui.edu.
المصدر: Mucosal immunology [Mucosal Immunol] 2024 Aug; Vol. 17 (4), pp. 537-553. Date of Electronic Publication: 2024 Mar 15.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Elsevier Country of Publication: United States NLM ID: 101299742 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1935-3456 (Electronic) Linking ISSN: 19330219 NLM ISO Abbreviation: Mucosal Immunol Subsets: MEDLINE
أسماء مطبوعة: Publication: 2023- : [New York, NY] : Elsevier
Original Publication: New York, NY : Nature Pub. Group, c2008-
مواضيع طبية MeSH: Asthma*/immunology , Asthma*/metabolism , Tumor Necrosis Factor Ligand Superfamily Member 15*/metabolism , Tumor Necrosis Factor Ligand Superfamily Member 15*/genetics , Disease Models, Animal* , Interleukin-9*/metabolism , Interleukin-9*/genetics, Animals ; Mice ; T-Lymphocytes, Helper-Inducer/immunology ; Humans ; Phenotype ; Receptors, Tumor Necrosis Factor, Member 25/metabolism ; Receptors, Tumor Necrosis Factor, Member 25/genetics ; Signal Transduction ; Cytokines/metabolism ; Interleukin-13/metabolism ; Mice, Knockout ; Inflammation/immunology ; Cells, Cultured
مستخلص: Multi-cytokine-producing Th9 cells secrete IL-9 and type 2 cytokines and mediate mouse and human allergic inflammation. However, the cytokines that promote a multi-cytokine secreting phenotype have not been defined. Tumor necrosis factor superfamily member TL1A signals through its receptor DR3 to increase IL-9. Here we demonstrate that TL1A increases expression of IL-9 and IL-13 co-expressing cells in murine Th9 cell cultures, inducing a multi-cytokine phenotype. Mechanistically, this is linked to histone modifications allowing for increased accessibility at the Il9 and Il13 loci. We further show that TL1A alters the transcription factor network underlying expression of IL-9 and IL-13 in Th9 cells and increases binding of transcription factors to Il9 and Il13 loci. TL1A-priming enhances the pathogenicity of Th9 cells in murine models of allergic airway disease through the increased expression of IL-9 and IL-13. Lastly, in both chronic and memory-recall models of allergic airway disease, blockade of TL1A signaling decreases the multi-cytokine Th9 cell population and attenuates the allergic phenotype. Taken together, these data demonstrate that TL1A promotes the development of multi-cytokine Th9 cells that drive allergic airway diseases and that targeting pathogenic T helper cell-promoting cytokines could be an effective approach for modifying disease.
(Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.)
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معلومات مُعتمدة: T32 HL007910 United States HL NHLBI NIH HHS; F30 AI174762 United States AI NIAID NIH HHS; P30 CA082709 United States CA NCI NIH HHS; T32 AI060519 United States AI NIAID NIH HHS; R01 AI057459 United States AI NIAID NIH HHS; U54 DK106846 United States DK NIDDK NIH HHS; T32 HL091816 United States HL NHLBI NIH HHS
المشرفين على المادة: 0 (Tumor Necrosis Factor Ligand Superfamily Member 15)
0 (Interleukin-9)
0 (Receptors, Tumor Necrosis Factor, Member 25)
0 (Tnfsf15 protein, mouse)
0 (Cytokines)
0 (Interleukin-13)
تواريخ الأحداث: Date Created: 20240317 Date Completed: 20240812 Latest Revision: 20240829
رمز التحديث: 20240830
مُعرف محوري في PubMed: PMC11354665
DOI: 10.1016/j.mucimm.2024.03.006
PMID: 38493956
قاعدة البيانات: MEDLINE
الوصف
تدمد:1935-3456
DOI:10.1016/j.mucimm.2024.03.006