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Prostaglandin E-2 suppresses human group 2 innate lymphoid cell function
Med Univ Graz, Inst Expt & Clin Pharmacol, Graz, Austria;Karolinska Inst, Dept Med Huddinge, Ctr Infect Med, Stockholm, Sweden.
Karolinska Inst, Dept Med, Immunol & Allergy Unit, Stockholm, Sweden.
Karolinska Inst, Dept Med Huddinge, Ctr Infect Med, Stockholm, Sweden.
Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Cell and Molecular Biology, Molecular Evolution. Uppsala University, Science for Life Laboratory, SciLifeLab.
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2018 (English)In: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 141, no 5, p. 1761-1773.e6Article in journal (Refereed) Published
Abstract [en]

Background: Group 2 innate lymphoid cells (ILC2s) are involved in the initial phase of type 2 inflammation and can amplify allergic immune responses by orchestrating other type 2 immune cells. Prostaglandin (PG) E-2 is a bioactive lipid that plays protective roles in the lung, particularly during allergic inflammation.

Objective: We set out to investigate how PGE(2) regulates human ILC2 function.

Methods: The effects of PGE(2) on human ILC2 proliferation and intracellular cytokine and transcription factor expression were assessed by means of flow cytometry. Cytokine production was measured by using ELISA, and real-time quantitative PCR was performed to detect PGE(2) receptor expression.

Results: PGE(2) inhibited GATA-3 expression, as well as production of the type 2 cytokines IL-5 and IL-13, from human tonsillar and blood ILC2s in response to stimulation with a combination of IL-25, IL-33, thymic stromal lymphopoietin, and IL-2. Furthermore, PGE(2) downregulated the expression of IL-2 receptor alpha (CD25). In line with this observation, PGE(2) decreased ILC2 proliferation. These effects were mediated by the combined action of E-type prostanoid receptor (EP) 2 and EP4 receptors, which were specifically expressed on ILC2s.

Conclusion: Our findings reveal that PGE(2) limits ILC2 activation and propose that selective EP2 and EP4 receptor agonists might serve as a promising therapeutic approach in treating allergic diseases by suppressing ILC2 function.

Place, publisher, year, edition, pages
MOSBY-ELSEVIER , 2018. Vol. 141, no 5, p. 1761-1773.e6
Keywords [en]
ILC2, allergy, prostaglandin E-2, E-type prostanoid receptor 2, E-type prostanoid receptor 4
National Category
Immunology Immunology in the medical area
Identifiers
URN: urn:nbn:se:uu:diva-356458DOI: 10.1016/j.jaci.2017.09.050ISI: 000432148200023PubMedID: 29217133OAI: oai:DiVA.org:uu-356458DiVA, id: diva2:1236106
Funder
Swedish Research Council, 521-2013-2791Swedish Foundation for Strategic Research , ICA12-0023Swedish Cancer Society, 130396Swedish Society for Medical Research (SSMF)Available from: 2018-07-31 Created: 2018-07-31 Last updated: 2018-10-30Bibliographically approved

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