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Cytokine-induced endogenous production of prostaglandin D-2 is essential for human group 2 innate lymphoid cell activation
Med Univ Graz, Austria; BioTechMed, Austria; Karolinska Inst, Sweden.
Karolinska Inst, Sweden; Karolinska Univ Hosp, Sweden.
Karolinska Inst, Sweden.
Karolinska Inst, Sweden.
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2019 (English)In: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 143, no 6, p. 2202-+Article in journal (Refereed) Published
Abstract [en]

Objective: We set out to examine PG production in human ILC2s and the implications of such endogenous production on ILC2 function. Methods: The effects of the COX-1/2 inhibitor flurbiprofen, the hematopoietic prostaglandin D2 synthase (HPGDS) inhibitor KMN698, and the CRTH2 antagonist CAY10471 on human ILC2s were determined by assessing receptor and transcription factor expression, cytokine production, and gene expression with flow cytometry, ELISA, and quantitative RT-PCR, respectively. Concentrations of lipid mediators were measured by using liquid chromatography-tandem mass spectrometry and ELISA. Results: We show that ILC2s constitutively express HPGDS and upregulate COX-2 upon IL-2, IL-25, and IL-33 plus thymic stromal lymphopoietin stimulation. Consequently, PGD2 and its metabolites can be detected in ILC2 supernatants. We reveal that endogenously produced PGD2 is essential in cytokine-induced ILC2 activation because blocking of the COX-1/2 or HPGDS enzymes or the CRTH2 receptor abolishes ILC2 responses. Conclusion: PGD2 produced by ILC2s is, in a paracrine/autocrine manner, essential in cytokine-induced ILC2 activation. Hence we provide the detailed mechanism behind how CRTH2 antagonists represent promising therapeutic tools for allergic diseases by controlling ILC2 function.

Place, publisher, year, edition, pages
MOSBY-ELSEVIER , 2019. Vol. 143, no 6, p. 2202-+
Keywords [en]
Group 2 innate lymphoid cells; prostaglandin D-2; chemoattractant receptor-homologous molecule expressed on T(H)2 cells; allergy
National Category
Medicinal Chemistry
Identifiers
URN: urn:nbn:se:liu:diva-158556DOI: 10.1016/j.jaci.2018.10.069ISI: 000470113200024PubMedID: 30578872OAI: oai:DiVA.org:liu-158556DiVA, id: diva2:1334895
Note

Funding Agencies|Swedish Research Council [521-2013-2791]; Swedish Cancer Society [130396]; Foundation for Strategic Research [ICA120023]; Swedish Society for Medical Research; Austrian Science Fund FWF [P25531-B23]; PhD Program DK-MOLIN [FWF-W1241]; Deutsche Forschungsgemeinschaft DFG [SFB 1039]; Swedish Research Council; Swedish Heart-Lung Foundation [HLF 20150640, HLF 20140469]; Swedish Heart-Lung Foundation; Karolinska Institutet; Vardal Foundation; Science for Life Laboratory Joint Research Collaboration; Karin and Sten Morstedt Initiative on Anaphylaxis; Swedish Foundation for Strategic Research

Available from: 2019-07-03 Created: 2019-07-03 Last updated: 2019-07-03

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Division of Surgery, Orthopedics and OncologyFaculty of Medicine and Health Sciences
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