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Bone marrow type 2 innate lymphoid cells: a local source of interleukin-5 in interleukin-33-driven eosinophilia

Journal article
Authors Kristina Johansson
Carina Malmhäll
Patricia Ramos-Ramírez
Madeleine Rådinger
Published in Immunology
Volume 153
Issue 2
Pages 268-278
ISSN 0019-2805
Publication year 2018
Published at Institute of Medicine, Department of Internal Medicine and Clinical Nutrition
Pages 268-278
Language en
Links dx.doi.org/10.1111/imm.12842
Keywords bone marrow, eosinophilia, IL-33, IL-5, ILC2, allergic airway inflammation, il-5 receptor-alpha, cd34(+) cells, asthmatic subjects, lung inflammation, induced increases, in-vivo, expression, hematopoiesis, mechanism, Immunology
Subject categories Internal medicine

Abstract

T helper type 2 (Th2) cells, type 2 innate lymphoid cells (ILC2s) and eosinophil progenitors have previously been described to produce interleukin-5 (IL-5) in the airways upon allergen provocation or by direct administration of IL-33. Eosinophilic airway inflammation is known to be associated with IL-5-dependent eosinophil development in the bone marrow, however, the source of IL-5 remains unclear. T helper cells, ILC2s and CD34(+) progenitors have been proposed to be involved in this process, therefore, we investigated whether these cells are taking part in eosinophilopoiesis by producing IL-5 locally in the bone marrow in IL-33-driven inflammation. Airway exposure with IL-33 led to eosinophil infiltration in airways and elevated eotaxin-2/CCL24. Importantly, IL-5 production as well as expression of the IL-33 receptor increased in ILC2s in the bone marrow under this treatment. A small but significant induction of IL-5 was also found in CD34(+) progenitors but not in T helper cells. Similar results were obtained by in vitro stimulation with IL-33 where ILC2s rapidly produced large amounts of IL-5, which coincided with the induction of eosinophil hematopoiesis. IL-33-mediated eosinophil production was indeed dependent on IL-5 as both airway and bone marrow eosinophils decreased in mice treated with anti-IL-5 in combination with IL-33. Interestingly, the responsiveness of ILC2s to IL-33 as well as IL-33-induced eotaxin-2/CCL24 were independent of the levels of IL-5. In summary, we demonstrate for the first time that IL-33 acts directly on bone marrow ILC2s, making them an early source of IL-5 and part of a process that is central in IL-33-driven eosinophilia.

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