دورية أكاديمية
E-Protein Inhibition in ILC2 Development Shapes the Function of Mature ILC2s during Allergic Airway Inflammation.
| العنوان: | E-Protein Inhibition in ILC2 Development Shapes the Function of Mature ILC2s during Allergic Airway Inflammation. |
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| المؤلفون: | Barshad G; Baker Institute for Animal Health, Cornell University College of Veterinary Medicine, Ithaca, NY.; Department of Biomedical Sciences, Cornell University College of Veterinary Medicine, Ithaca, NY., Webb LM; Department of Immunology, University of Washington, Seattle, WA; lwebb2@uw.edu etwojno@uw.edu., Ting HA; Department of Immunology, University of Washington, Seattle, WA., Oyesola OO; Department of Immunology, University of Washington, Seattle, WA., Onyekwere OG; Baker Institute for Animal Health, Cornell University College of Veterinary Medicine, Ithaca, NY.; Department of Microbiology and Immunology, Cornell University College of Veterinary Medicine, Ithaca, NY; and., Lewis JJ; Baker Institute for Animal Health, Cornell University College of Veterinary Medicine, Ithaca, NY.; Department of Biomedical Sciences, Cornell University College of Veterinary Medicine, Ithaca, NY., Rice EJ; Baker Institute for Animal Health, Cornell University College of Veterinary Medicine, Ithaca, NY.; Department of Biomedical Sciences, Cornell University College of Veterinary Medicine, Ithaca, NY., Matheson MK; Department of Immunology, University of Washington, Seattle, WA., Sun XH; Arthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK., von Moltke J; Department of Immunology, University of Washington, Seattle, WA., Danko CG; Baker Institute for Animal Health, Cornell University College of Veterinary Medicine, Ithaca, NY.; Department of Biomedical Sciences, Cornell University College of Veterinary Medicine, Ithaca, NY., Tait Wojno ED; Department of Immunology, University of Washington, Seattle, WA; lwebb2@uw.edu etwojno@uw.edu. |
| المصدر: | Journal of immunology (Baltimore, Md. : 1950) [J Immunol] 2022 Mar 01; Vol. 208 (5), pp. 1007-1020. Date of Electronic Publication: 2022 Feb 18. |
| نوع المنشور: | Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: American Association of Immunologists Country of Publication: United States NLM ID: 2985117R Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1550-6606 (Electronic) Linking ISSN: 00221767 NLM ISO Abbreviation: J Immunol Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: Bethesda, MD : American Association of Immunologists Original Publication: Baltimore : Williams & Wilkins, c1950- |
| مواضيع طبية MeSH: | Antigens, Dermatophagoides/*immunology , Asthma/*immunology , Inhibitor of Differentiation Protein 1/*metabolism , T-Lymphocytes/*immunology , Transcription Factors/*metabolism, Adaptor Proteins, Signal Transducing/genetics ; Allergens/immunology ; Animals ; Asthma/pathology ; Cell Differentiation/immunology ; Chromatin/metabolism ; Cytokines/immunology ; DNA-Binding Proteins/antagonists & inhibitors ; Female ; Lectins, C-Type/genetics ; Lung/immunology ; Lung/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Pyroglyphidae/immunology ; Receptors, Immunologic/genetics ; Stem Cells/cytology ; T-Lymphocytes/cytology ; Transcription Factor AP-1/metabolism |
| مستخلص: | E-protein transcription factors limit group 2 innate lymphoid cell (ILC2) development while promoting T cell differentiation from common lymphoid progenitors. Inhibitors of DNA binding (ID) proteins block E-protein DNA binding in common lymphoid progenitors to allow ILC2 development. However, whether E-proteins influence ILC2 function upon maturity and activation remains unclear. Mice that overexpress ID1 under control of the thymus-restricted proximal Lck promoter (ID1 tg/WT ) have a large pool of primarily thymus-derived ILC2s in the periphery that develop in the absence of E-protein activity. We used these mice to investigate how the absence of E-protein activity affects ILC2 function and the genomic landscape in response to house dust mite (HDM) allergens. ID1 tg/WT mice had increased KLRG1 - ILC2s in the lung compared with wild-type (WT; ID1 WT/WT ) mice in response to HDM, but ID1 tg/WT ILC2s had an impaired capacity to produce type 2 cytokines. Analysis of WT ILC2 accessible chromatin suggested that AP-1 and C/EBP transcription factors but not E-proteins were associated with ILC2 inflammatory gene programs. Instead, E-protein binding sites were enriched at functional genes in ILC2s during development that were later dynamically regulated in allergic lung inflammation, including genes that control ILC2 response to cytokines and interactions with T cells. Finally, ILC2s from ID1 tg/WT compared with WT mice had fewer regions of open chromatin near functional genes that were enriched for AP-1 factor binding sites following HDM treatment. These data show that E-proteins shape the chromatin landscape during ILC2 development to dictate the functional capacity of mature ILC2s during allergic inflammation in the lung. (Copyright © 2022 by The American Association of Immunologists, Inc.) |
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| معلومات مُعتمدة: | DP2 AI136596 United States AI NIAID NIH HHS; R01 HG010346 United States HG NHGRI NIH HHS; S10 OD024979 United States OD NIH HHS; K22 AI116729 United States AI NIAID NIH HHS; R01 AI132708 United States AI NIAID NIH HHS; R01 AI130379 United States AI NIAID NIH HHS; R01 AI126851 United States AI NIAID NIH HHS |
| المشرفين على المادة: | 0 (Adaptor Proteins, Signal Transducing) 0 (Allergens) 0 (Antigens, Dermatophagoides) 0 (Chromatin) 0 (Cytokines) 0 (DNA-Binding Proteins) 0 (Idb1 protein, mouse) 0 (Inhibitor of Differentiation Protein 1) 0 (Klrg1 protein, mouse) 0 (Lectins, C-Type) 0 (Receptors, Immunologic) 0 (Sh2d2a protein, mouse) 0 (Transcription Factor AP-1) 0 (Transcription Factors) |
| تواريخ الأحداث: | Date Created: 20220219 Date Completed: 20220307 Latest Revision: 20221007 |
| رمز التحديث: | 20221213 |
| مُعرف محوري في PubMed: | PMC8881320 |
| DOI: | 10.4049/jimmunol.2100414 |
| PMID: | 35181641 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 1550-6606 |
|---|---|
| DOI: | 10.4049/jimmunol.2100414 |