Semaphorin 3E deficiency dysregulates dendritic cell functions: In vitro and in vivo evidence.

Regulation of dendritic cell functions is a complex process in which several mediators play diverse roles as a network in a context-dependent manner. The precise mechanisms underlying dendritic cell functions have remained to be addressed. Semaphorins play crucial roles in regulation of various cell...

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Autores principales:	Hesam Movassagh, Lianyu Shan, Latifa Koussih, Abdulaziz Alamri, Nazila Ariaee, Sam K P Kung, Abdelilah S Gounni
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/3d4a970dab344957a40f014fb329ce8e
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spelling	oai:doaj.org-article:3d4a970dab344957a40f014fb329ce8e2021-12-02T20:09:52ZSemaphorin 3E deficiency dysregulates dendritic cell functions: In vitro and in vivo evidence.1932-620310.1371/journal.pone.0252868https://doaj.org/article/3d4a970dab344957a40f014fb329ce8e2021-01-01T00:00:00Zhttps://doi.org/10.1371/journal.pone.0252868https://doaj.org/toc/1932-6203Regulation of dendritic cell functions is a complex process in which several mediators play diverse roles as a network in a context-dependent manner. The precise mechanisms underlying dendritic cell functions have remained to be addressed. Semaphorins play crucial roles in regulation of various cell functions. We previously revealed that Semaphorin 3E (Sema3E) contributes to regulation of allergen-induced airway pathology partly mediated by controlling recruitment of conventional dendritic cell subsets in vivo, though the underlying mechanism remained elusive. In this study, we investigate the potential regulatory role of Sema3E in dendritic cells. We demonstrated that bone marrow-derived dendritic cells differentiated from Sema3e-/- progenitors have an enhanced migration capacity both at the baseline and in response to CCL21. The enhanced migration ability of Sema3E dendritic cells was associated with an overexpression of the chemokine receptor (CCR7), elevated Rac1 GTPase activity and F-actin polymerization. Using a mouse model of allergic airway sensitization, we observed that genetic deletion of Sema3E leads to a time dependent upregulation of CCR7 on CD11b+ conventional dendritic cells in the lungs and mediastinal lymph nodes. Furthermore, aeroallergen sensitization of Sema3e-/- mice lead to an enhanced expression of PD-L2 and IRF-4 as well as enhanced allergen uptake in pulmonary CD11b+ DC, compared to wild type littermates. Collectively, these data suggest that Sema3E implicates in regulation of dendritic cell functions which could be considered a basis for novel immunotherapeutic strategies for the diseases associated with defective dendritic cells in the future.Hesam MovassaghLianyu ShanLatifa KoussihAbdulaziz AlamriNazila AriaeeSam K P KungAbdelilah S GounniPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 16, Iss 6, p e0252868 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Hesam Movassagh Lianyu Shan Latifa Koussih Abdulaziz Alamri Nazila Ariaee Sam K P Kung Abdelilah S Gounni Semaphorin 3E deficiency dysregulates dendritic cell functions: In vitro and in vivo evidence.
description	Regulation of dendritic cell functions is a complex process in which several mediators play diverse roles as a network in a context-dependent manner. The precise mechanisms underlying dendritic cell functions have remained to be addressed. Semaphorins play crucial roles in regulation of various cell functions. We previously revealed that Semaphorin 3E (Sema3E) contributes to regulation of allergen-induced airway pathology partly mediated by controlling recruitment of conventional dendritic cell subsets in vivo, though the underlying mechanism remained elusive. In this study, we investigate the potential regulatory role of Sema3E in dendritic cells. We demonstrated that bone marrow-derived dendritic cells differentiated from Sema3e-/- progenitors have an enhanced migration capacity both at the baseline and in response to CCL21. The enhanced migration ability of Sema3E dendritic cells was associated with an overexpression of the chemokine receptor (CCR7), elevated Rac1 GTPase activity and F-actin polymerization. Using a mouse model of allergic airway sensitization, we observed that genetic deletion of Sema3E leads to a time dependent upregulation of CCR7 on CD11b+ conventional dendritic cells in the lungs and mediastinal lymph nodes. Furthermore, aeroallergen sensitization of Sema3e-/- mice lead to an enhanced expression of PD-L2 and IRF-4 as well as enhanced allergen uptake in pulmonary CD11b+ DC, compared to wild type littermates. Collectively, these data suggest that Sema3E implicates in regulation of dendritic cell functions which could be considered a basis for novel immunotherapeutic strategies for the diseases associated with defective dendritic cells in the future.
format	article
author	Hesam Movassagh Lianyu Shan Latifa Koussih Abdulaziz Alamri Nazila Ariaee Sam K P Kung Abdelilah S Gounni
author_facet	Hesam Movassagh Lianyu Shan Latifa Koussih Abdulaziz Alamri Nazila Ariaee Sam K P Kung Abdelilah S Gounni
author_sort	Hesam Movassagh
title	Semaphorin 3E deficiency dysregulates dendritic cell functions: In vitro and in vivo evidence.
title_short	Semaphorin 3E deficiency dysregulates dendritic cell functions: In vitro and in vivo evidence.
title_full	Semaphorin 3E deficiency dysregulates dendritic cell functions: In vitro and in vivo evidence.
title_fullStr	Semaphorin 3E deficiency dysregulates dendritic cell functions: In vitro and in vivo evidence.
title_full_unstemmed	Semaphorin 3E deficiency dysregulates dendritic cell functions: In vitro and in vivo evidence.
title_sort	semaphorin 3e deficiency dysregulates dendritic cell functions: in vitro and in vivo evidence.
publisher	Public Library of Science (PLoS)
publishDate	2021
url	https://doaj.org/article/3d4a970dab344957a40f014fb329ce8e
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Semaphorin 3E deficiency dysregulates dendritic cell functions: In vitro and in vivo evidence.

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