Prostaglandin E2-EP3 axis in fine-tuning excessive skin inflammation by restricting dendritic cell functions.

Prostaglandin E2 (PGE2) is produced in the skin and is suggested to play a role in the regulation of cutaneous immune homeostasis and responses. However, the multifaceted functions of PGE2 continue to elude our understanding, especially because of the multiplicity of PGE2 receptors--EP1, EP2, EP3, a...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Noriko Shiraishi, Takashi Nomura, Hideaki Tanizaki, Saeko Nakajima, Shuh Narumiya, Yoshiki Miyachi, Yoshiki Tokura, Kenji Kabashima
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/b938c1fb4df643e4ad15fe2045295303
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:b938c1fb4df643e4ad15fe2045295303
record_format	dspace
spelling	oai:doaj.org-article:b938c1fb4df643e4ad15fe20452953032021-11-18T09:02:26ZProstaglandin E2-EP3 axis in fine-tuning excessive skin inflammation by restricting dendritic cell functions.1932-620310.1371/journal.pone.0069599https://doaj.org/article/b938c1fb4df643e4ad15fe20452953032013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23922752/?tool=EBIhttps://doaj.org/toc/1932-6203Prostaglandin E2 (PGE2) is produced in the skin and is suggested to play a role in the regulation of cutaneous immune homeostasis and responses. However, the multifaceted functions of PGE2 continue to elude our understanding, especially because of the multiplicity of PGE2 receptors--EP1, EP2, EP3, and EP4. While cAMP-elevating EP4 is known to activate the functions of cutaneous dendritic cells (DCs), including Langerhans cells (LCs) and dermal DCs, the role of cAMP-suppressing EP3 in this process remains unknown. Here we demonstrated that an EP3 receptor selective agonist, ONO-AE-248, inhibited chemotaxis and co-stimulatory molecule expressions of DCs in vitro. A suboptimal dose of antigen was sufficient to induce contact hypersensitivity in EP3-deficient mice. Intriguingly, EP3 deficiency did not impair skin inflammation at all when the antigen dose was sufficiently high. EP3 limited the functions of cutaneous DCs only when the antigen dose was low. In contrast to EP4, the observed unappreciated function of EP3 may stabilize the cutaneous DCs to halt the impetuous response to a suboptimal dose of antigen. Taken together, PGE2-EP3 signaling is essential for fine-tuning excessive skin inflammation by restricting DC functions.Noriko ShiraishiTakashi NomuraHideaki TanizakiSaeko NakajimaShuh NarumiyaYoshiki MiyachiYoshiki TokuraKenji KabashimaPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 7, p e69599 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Noriko Shiraishi Takashi Nomura Hideaki Tanizaki Saeko Nakajima Shuh Narumiya Yoshiki Miyachi Yoshiki Tokura Kenji Kabashima Prostaglandin E2-EP3 axis in fine-tuning excessive skin inflammation by restricting dendritic cell functions.
description	Prostaglandin E2 (PGE2) is produced in the skin and is suggested to play a role in the regulation of cutaneous immune homeostasis and responses. However, the multifaceted functions of PGE2 continue to elude our understanding, especially because of the multiplicity of PGE2 receptors--EP1, EP2, EP3, and EP4. While cAMP-elevating EP4 is known to activate the functions of cutaneous dendritic cells (DCs), including Langerhans cells (LCs) and dermal DCs, the role of cAMP-suppressing EP3 in this process remains unknown. Here we demonstrated that an EP3 receptor selective agonist, ONO-AE-248, inhibited chemotaxis and co-stimulatory molecule expressions of DCs in vitro. A suboptimal dose of antigen was sufficient to induce contact hypersensitivity in EP3-deficient mice. Intriguingly, EP3 deficiency did not impair skin inflammation at all when the antigen dose was sufficiently high. EP3 limited the functions of cutaneous DCs only when the antigen dose was low. In contrast to EP4, the observed unappreciated function of EP3 may stabilize the cutaneous DCs to halt the impetuous response to a suboptimal dose of antigen. Taken together, PGE2-EP3 signaling is essential for fine-tuning excessive skin inflammation by restricting DC functions.
format	article
author	Noriko Shiraishi Takashi Nomura Hideaki Tanizaki Saeko Nakajima Shuh Narumiya Yoshiki Miyachi Yoshiki Tokura Kenji Kabashima
author_facet	Noriko Shiraishi Takashi Nomura Hideaki Tanizaki Saeko Nakajima Shuh Narumiya Yoshiki Miyachi Yoshiki Tokura Kenji Kabashima
author_sort	Noriko Shiraishi
title	Prostaglandin E2-EP3 axis in fine-tuning excessive skin inflammation by restricting dendritic cell functions.
title_short	Prostaglandin E2-EP3 axis in fine-tuning excessive skin inflammation by restricting dendritic cell functions.
title_full	Prostaglandin E2-EP3 axis in fine-tuning excessive skin inflammation by restricting dendritic cell functions.
title_fullStr	Prostaglandin E2-EP3 axis in fine-tuning excessive skin inflammation by restricting dendritic cell functions.
title_full_unstemmed	Prostaglandin E2-EP3 axis in fine-tuning excessive skin inflammation by restricting dendritic cell functions.
title_sort	prostaglandin e2-ep3 axis in fine-tuning excessive skin inflammation by restricting dendritic cell functions.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/b938c1fb4df643e4ad15fe2045295303
work_keys_str_mv	AT norikoshiraishi prostaglandine2ep3axisinfinetuningexcessiveskininflammationbyrestrictingdendriticcellfunctions AT takashinomura prostaglandine2ep3axisinfinetuningexcessiveskininflammationbyrestrictingdendriticcellfunctions AT hideakitanizaki prostaglandine2ep3axisinfinetuningexcessiveskininflammationbyrestrictingdendriticcellfunctions AT saekonakajima prostaglandine2ep3axisinfinetuningexcessiveskininflammationbyrestrictingdendriticcellfunctions AT shuhnarumiya prostaglandine2ep3axisinfinetuningexcessiveskininflammationbyrestrictingdendriticcellfunctions AT yoshikimiyachi prostaglandine2ep3axisinfinetuningexcessiveskininflammationbyrestrictingdendriticcellfunctions AT yoshikitokura prostaglandine2ep3axisinfinetuningexcessiveskininflammationbyrestrictingdendriticcellfunctions AT kenjikabashima prostaglandine2ep3axisinfinetuningexcessiveskininflammationbyrestrictingdendriticcellfunctions
_version_	1718420987357167616

Prostaglandin E2-EP3 axis in fine-tuning excessive skin inflammation by restricting dendritic cell functions.

Ejemplares similares