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Editorial
. 2022 Sep;150(3):585-586.
doi: 10.1016/j.jaci.2022.05.015. Epub 2022 Jun 2.

Insights into the biology of IL-9 in asthma

Affiliations
Editorial

Insights into the biology of IL-9 in asthma

Taylor A Doherty et al. J Allergy Clin Immunol. 2022 Sep.
No abstract available

Keywords: IL-9; arginase-1; asthma; macrophages.

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Conflict of interest statement

Disclosure of potential conflict of interest: The authors declare that they have no relevant conflicts of interest.

Figures

FIG 1.
FIG 1.
The IL-9/Arg1/CCL5 axis in type 2 lung inflammation. Allergens, including house dust mite and Aspergillus species, induce the alarmins thymic stromal lymphopoietin (TSLP) and IL-33, which promote IL-9 production from group 2 innate lymphocytes (ILC2s). IL-9 can also be secreted from CD4+ TH2 or TH9 cells. IL-9 is known to induce mast cell accumulation, and recent work by Fu et al demonstrated that IL-9 induces high levels of Arg1 in lung IMs, which is required for maximal CCL5 chemokine secretion. CCL5 then recruits eosinophils, T cells, and monocytes into the lung to propagate type 2 inflammation. ILC2s and TH2 cells also produce IL-5, which stimulates eosinophil egress from bone marrow, and IL-13, which promotes mucus production, airway hyperresponsiveness (AHR), and remodeling.

Comment on

  • An IL-9-pulmonary macrophage axis defines the allergic lung inflammatory environment.
    Fu Y, Wang J, Zhou B, Pajulas A, Gao H, Ramdas B, Koh B, Ulrich BJ, Yang S, Kapur R, Renauld JC, Paczesny S, Liu Y, Tighe RM, Licona-Limón P, Flavell RA, Takatsuka S, Kitamura D, Tepper RS, Sun J, Kaplan MH. Fu Y, et al. Sci Immunol. 2022 Feb 18;7(68):eabi9768. doi: 10.1126/sciimmunol.abi9768. Epub 2022 Feb 18. Sci Immunol. 2022. PMID: 35179949 Free PMC article.

References

    1. Erpenbeck VJ, Hohlfeld JM, Volkmann B, Hagenberg A, Geldmacher H, Braun A, et al. Segmental allergen challenge in patients with atopic asthma leads to increased IL-9 expression in bronchoalveolar lavage fluid lymphocytes. J Allergy Clin Immunol 2003;111:1319–27. - PubMed
    1. Shimbara A, Christodoulopoulos P, Soussi-Gounni A, Olivenstein R, Nakamura Y, Levitt RC, et al. IL-9 and its receptor in allergic and nonallergic lung disease: increased expression in asthma. J Allergy Clin Immunol 2000;105:108–15. - PubMed
    1. Chakraborty S, Kubatzky KF, Mitra DK. An update on interleukin-9: from its cellular source and signal transduction to its role in immunopathogenesis. Int J Mol Sci 2019;20:2113. - PMC - PubMed
    1. Temann UA, Geba GP, Rankin JA, Flavell RA. Expression of interleukin 9 in the lungs of transgenic mice causes airway inflammation, mast cell hyperplasia, and bronchial hyperresponsiveness. J Exp Med 1998;188:1307–20. - PMC - PubMed
    1. Fu Y, Wang J, Zhou B, Pajulas A, Gao H, Ramdas B, et al. An IL-9–pulmonary macrophage axis defines the allergic lung inflammatory environment. Sci Immunol 2022;7:eabi9768. - PMC - PubMed

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