Prostaglandin E2 down-regulates the expression of CD25 on bovine T cells, and this effect is mediated through the EP4 receptor

Maślanka, Tomasz; Spodniewska, A.; Barski, D.; Jasiecka, Agnieszka; Zuśka-Prot, Monika; Ziółkowski, Hubert; Markiewicz, W.; Jaroszewski, Jerzy Jan

doi:10.1016/j.vetimm.2014.05.003

Cited by 18 publications

(11 citation statements)

References 23 publications

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“…These data are in line with previous reports demonstrating that PGE 2 reduces CD25 expression and, consequently, IL-2 signaling in human primary peripheral blood T cells 63 and bovine CD4 + T cells. 64 Similarly, PGE 2 was previously shown to induce genes that block the cell cycle and proliferation of human primary CD4 + T cells. 42 , 65 …”

Section: Discussionmentioning

confidence: 93%

Prostaglandin E 2 suppresses human group 2 innate lymphoid cell function

Maric

Ravindran

Mazzurana

et al. 2018

Journal of Allergy and Clinical Immunology

126

102

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BackgroundGroup 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) E2 is a bioactive lipid that plays protective roles in the lung, particularly during allergic inflammation.ObjectiveWe set out to investigate how PGE2 regulates human ILC2 function.MethodsThe effects of PGE2 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 PGE2 receptor expression.ResultsPGE2 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, PGE2 downregulated the expression of IL-2 receptor α (CD25). In line with this observation, PGE2 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.ConclusionOur findings reveal that PGE2 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.

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Section: Discussionmentioning

confidence: 93%

Prostaglandin E 2 suppresses human group 2 innate lymphoid cell function

Maric

Ravindran

Mazzurana

et al. 2018

Journal of Allergy and Clinical Immunology

126

102

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“…Because all four EP receptors were shown to be expressed in neurons and induced in VECs under conditions of hypoxic–ischemic encephalopathy [ 38 ], EP receptors are known to be inducible in pathological conditions. In previous studies, T cells were regulated by PGE 2 , and this effect was mediated by EP2 or EP4 [ 39 , 40 , 41 ]. Moreover, IL-1β upregulated EP2 and EP4 in primary cultured hippocampal neurons [ 42 ].…”

Section: Discussionmentioning

confidence: 99%

Microsomal Prostaglandin E Synthase-1 Facilitates an Intercellular Interaction between CD4+ T Cells through IL-1β Autocrine Function in Experimental Autoimmune Encephalomyelitis

Takemiya

Takeuchi

Kawakami

2017

IJMS

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Microsomal prostaglandin synthetase-1 (mPGES-1) is an inducible terminal enzyme that produces prostaglandin E2 (PGE2). In our previous study, we investigated the role of mPGES-1 in the inflammation and demyelination observed in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis, using mPGES-1-deficient (mPGES-1−/−) and wild-type (wt) mice. We found that mPGES-1 facilitated inflammation, demyelination, and paralysis and was induced in vascular endothelial cells and macrophages and microglia around inflammatory foci. Here, we investigated the role of interleukin-1β (IL-1β) in the intercellular mechanism stimulated by mPGES-1 in EAE spinal cords in the presence of inflammation. We found that the area invaded by CD4-positive (CD4+) T cells was extensive, and that PGE2 receptors EP1–4 were more induced in activated CD4+ T cells of wt mice than in those of mPGES-1−/− mice. Moreover, IL-1β and IL-1 receptor 1 (IL-1r1) were produced by 65% and 48% of CD4+ T cells in wt mice and by 44% and 27% of CD4+ T cells in mPGES-1−/− mice. Furthermore, interleukin-17 (IL-17) was released from the activated CD4+ T cells. Therefore, mPGES-1 stimulates an intercellular interaction between CD4+ T cells by upregulating the autocrine function of IL-1β in activated CD4+ T cells, which release IL-17 to facilitate axonal and myelin damage in EAE mice.

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“…The EP 2 and EP 4 activate G proteins that stimulate cAMP production by activating AC [Maślanka et al, 2014;Chen et al, 2010]. EP 4 is the main receptor involved in some inflammatory diseases [Xia et al, 2014].…”

Section: Introductionmentioning

confidence: 99%