Notch Signaling Regulates Immune Responses in Atherosclerosis

Atherosclerosis is a chronic autoimmune inflammatory disease that can cause coronary artery disease, stroke, peripheral artery disease, depending on which arteries are affected. At the beginning of atherosclerosis plasma lipoproteins accumulate in the sub-endothelial space. In response, monocytes mi...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Francesco Vieceli Dalla Sega [verfasserIn] Francesca Fortini [verfasserIn] Giorgio Aquila [verfasserIn] Gianluca Campo [verfasserIn] Mauro Vaccarezza [verfasserIn] Paola Rizzo [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2019

Schlagwörter:	atherosclerosis endothelial dysfunction Notch Dll4 immunity M1 macrophages

Übergeordnetes Werk:	In: Frontiers in Immunology - Frontiers Media S.A., 2011, 10(2019)
Übergeordnetes Werk:	volume:10 ; year:2019

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3389/fimmu.2019.01130

Katalog-ID:	DOAJ020324359

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520			\|a Atherosclerosis is a chronic autoimmune inflammatory disease that can cause coronary artery disease, stroke, peripheral artery disease, depending on which arteries are affected. At the beginning of atherosclerosis plasma lipoproteins accumulate in the sub-endothelial space. In response, monocytes migrate from the circulation through the endothelium into the intima where they differentiate into macrophages. These early events trigger a complex immune response that eventually involves many cellular subtypes of both innate and adaptive immunity. The Notch signaling pathway is an evolutionary conserved cell signaling system that mediates cell-to-cell communication. Recent studies have revealed that Notch modulate atherosclerosis by controlling macrophages polarization into M1 or M2 subtypes. Furthermore, it is known that Notch signaling controls differentiation and activity of T-helper and cytotoxic T-cells in inflammatory diseases. In this review, we will discuss the role of Notch in modulating immunity in the context of atherosclerosis and whether targeting Notch may represent a therapeutic strategy.
650		4	\|a atherosclerosis
650		4	\|a endothelial dysfunction
650		4	\|a Notch
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allfields	10.3389/fimmu.2019.01130 doi (DE-627)DOAJ020324359 (DE-599)DOAJ3b9a37a3ff1b4953827d137964d408b9 DE-627 ger DE-627 rakwb eng RC581-607 Francesco Vieceli Dalla Sega verfasserin aut Notch Signaling Regulates Immune Responses in Atherosclerosis 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Atherosclerosis is a chronic autoimmune inflammatory disease that can cause coronary artery disease, stroke, peripheral artery disease, depending on which arteries are affected. At the beginning of atherosclerosis plasma lipoproteins accumulate in the sub-endothelial space. In response, monocytes migrate from the circulation through the endothelium into the intima where they differentiate into macrophages. These early events trigger a complex immune response that eventually involves many cellular subtypes of both innate and adaptive immunity. The Notch signaling pathway is an evolutionary conserved cell signaling system that mediates cell-to-cell communication. Recent studies have revealed that Notch modulate atherosclerosis by controlling macrophages polarization into M1 or M2 subtypes. Furthermore, it is known that Notch signaling controls differentiation and activity of T-helper and cytotoxic T-cells in inflammatory diseases. In this review, we will discuss the role of Notch in modulating immunity in the context of atherosclerosis and whether targeting Notch may represent a therapeutic strategy. atherosclerosis endothelial dysfunction Notch Dll4 immunity M1 macrophages Immunologic diseases. Allergy Francesca Fortini verfasserin aut Giorgio Aquila verfasserin aut Gianluca Campo verfasserin aut Gianluca Campo verfasserin aut Mauro Vaccarezza verfasserin aut Paola Rizzo verfasserin aut Paola Rizzo verfasserin aut Paola Rizzo verfasserin aut In Frontiers in Immunology Frontiers Media S.A., 2011 10(2019) (DE-627)657998354 (DE-600)2606827-8 16643224 nnns volume:10 year:2019 https://doi.org/10.3389/fimmu.2019.01130 kostenfrei https://doaj.org/article/3b9a37a3ff1b4953827d137964d408b9 kostenfrei https://www.frontiersin.org/article/10.3389/fimmu.2019.01130/full kostenfrei https://doaj.org/toc/1664-3224 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2019
spelling	10.3389/fimmu.2019.01130 doi (DE-627)DOAJ020324359 (DE-599)DOAJ3b9a37a3ff1b4953827d137964d408b9 DE-627 ger DE-627 rakwb eng RC581-607 Francesco Vieceli Dalla Sega verfasserin aut Notch Signaling Regulates Immune Responses in Atherosclerosis 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Atherosclerosis is a chronic autoimmune inflammatory disease that can cause coronary artery disease, stroke, peripheral artery disease, depending on which arteries are affected. At the beginning of atherosclerosis plasma lipoproteins accumulate in the sub-endothelial space. In response, monocytes migrate from the circulation through the endothelium into the intima where they differentiate into macrophages. These early events trigger a complex immune response that eventually involves many cellular subtypes of both innate and adaptive immunity. The Notch signaling pathway is an evolutionary conserved cell signaling system that mediates cell-to-cell communication. Recent studies have revealed that Notch modulate atherosclerosis by controlling macrophages polarization into M1 or M2 subtypes. Furthermore, it is known that Notch signaling controls differentiation and activity of T-helper and cytotoxic T-cells in inflammatory diseases. In this review, we will discuss the role of Notch in modulating immunity in the context of atherosclerosis and whether targeting Notch may represent a therapeutic strategy. atherosclerosis endothelial dysfunction Notch Dll4 immunity M1 macrophages Immunologic diseases. Allergy Francesca Fortini verfasserin aut Giorgio Aquila verfasserin aut Gianluca Campo verfasserin aut Gianluca Campo verfasserin aut Mauro Vaccarezza verfasserin aut Paola Rizzo verfasserin aut Paola Rizzo verfasserin aut Paola Rizzo verfasserin aut In Frontiers in Immunology Frontiers Media S.A., 2011 10(2019) (DE-627)657998354 (DE-600)2606827-8 16643224 nnns volume:10 year:2019 https://doi.org/10.3389/fimmu.2019.01130 kostenfrei https://doaj.org/article/3b9a37a3ff1b4953827d137964d408b9 kostenfrei https://www.frontiersin.org/article/10.3389/fimmu.2019.01130/full kostenfrei https://doaj.org/toc/1664-3224 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2019
allfields_unstemmed	10.3389/fimmu.2019.01130 doi (DE-627)DOAJ020324359 (DE-599)DOAJ3b9a37a3ff1b4953827d137964d408b9 DE-627 ger DE-627 rakwb eng RC581-607 Francesco Vieceli Dalla Sega verfasserin aut Notch Signaling Regulates Immune Responses in Atherosclerosis 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Atherosclerosis is a chronic autoimmune inflammatory disease that can cause coronary artery disease, stroke, peripheral artery disease, depending on which arteries are affected. At the beginning of atherosclerosis plasma lipoproteins accumulate in the sub-endothelial space. In response, monocytes migrate from the circulation through the endothelium into the intima where they differentiate into macrophages. These early events trigger a complex immune response that eventually involves many cellular subtypes of both innate and adaptive immunity. The Notch signaling pathway is an evolutionary conserved cell signaling system that mediates cell-to-cell communication. Recent studies have revealed that Notch modulate atherosclerosis by controlling macrophages polarization into M1 or M2 subtypes. Furthermore, it is known that Notch signaling controls differentiation and activity of T-helper and cytotoxic T-cells in inflammatory diseases. In this review, we will discuss the role of Notch in modulating immunity in the context of atherosclerosis and whether targeting Notch may represent a therapeutic strategy. atherosclerosis endothelial dysfunction Notch Dll4 immunity M1 macrophages Immunologic diseases. Allergy Francesca Fortini verfasserin aut Giorgio Aquila verfasserin aut Gianluca Campo verfasserin aut Gianluca Campo verfasserin aut Mauro Vaccarezza verfasserin aut Paola Rizzo verfasserin aut Paola Rizzo verfasserin aut Paola Rizzo verfasserin aut In Frontiers in Immunology Frontiers Media S.A., 2011 10(2019) (DE-627)657998354 (DE-600)2606827-8 16643224 nnns volume:10 year:2019 https://doi.org/10.3389/fimmu.2019.01130 kostenfrei https://doaj.org/article/3b9a37a3ff1b4953827d137964d408b9 kostenfrei https://www.frontiersin.org/article/10.3389/fimmu.2019.01130/full kostenfrei https://doaj.org/toc/1664-3224 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2019
allfieldsGer	10.3389/fimmu.2019.01130 doi (DE-627)DOAJ020324359 (DE-599)DOAJ3b9a37a3ff1b4953827d137964d408b9 DE-627 ger DE-627 rakwb eng RC581-607 Francesco Vieceli Dalla Sega verfasserin aut Notch Signaling Regulates Immune Responses in Atherosclerosis 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Atherosclerosis is a chronic autoimmune inflammatory disease that can cause coronary artery disease, stroke, peripheral artery disease, depending on which arteries are affected. At the beginning of atherosclerosis plasma lipoproteins accumulate in the sub-endothelial space. In response, monocytes migrate from the circulation through the endothelium into the intima where they differentiate into macrophages. These early events trigger a complex immune response that eventually involves many cellular subtypes of both innate and adaptive immunity. The Notch signaling pathway is an evolutionary conserved cell signaling system that mediates cell-to-cell communication. Recent studies have revealed that Notch modulate atherosclerosis by controlling macrophages polarization into M1 or M2 subtypes. Furthermore, it is known that Notch signaling controls differentiation and activity of T-helper and cytotoxic T-cells in inflammatory diseases. In this review, we will discuss the role of Notch in modulating immunity in the context of atherosclerosis and whether targeting Notch may represent a therapeutic strategy. atherosclerosis endothelial dysfunction Notch Dll4 immunity M1 macrophages Immunologic diseases. Allergy Francesca Fortini verfasserin aut Giorgio Aquila verfasserin aut Gianluca Campo verfasserin aut Gianluca Campo verfasserin aut Mauro Vaccarezza verfasserin aut Paola Rizzo verfasserin aut Paola Rizzo verfasserin aut Paola Rizzo verfasserin aut In Frontiers in Immunology Frontiers Media S.A., 2011 10(2019) (DE-627)657998354 (DE-600)2606827-8 16643224 nnns volume:10 year:2019 https://doi.org/10.3389/fimmu.2019.01130 kostenfrei https://doaj.org/article/3b9a37a3ff1b4953827d137964d408b9 kostenfrei https://www.frontiersin.org/article/10.3389/fimmu.2019.01130/full kostenfrei https://doaj.org/toc/1664-3224 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2019
allfieldsSound	10.3389/fimmu.2019.01130 doi (DE-627)DOAJ020324359 (DE-599)DOAJ3b9a37a3ff1b4953827d137964d408b9 DE-627 ger DE-627 rakwb eng RC581-607 Francesco Vieceli Dalla Sega verfasserin aut Notch Signaling Regulates Immune Responses in Atherosclerosis 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Atherosclerosis is a chronic autoimmune inflammatory disease that can cause coronary artery disease, stroke, peripheral artery disease, depending on which arteries are affected. At the beginning of atherosclerosis plasma lipoproteins accumulate in the sub-endothelial space. In response, monocytes migrate from the circulation through the endothelium into the intima where they differentiate into macrophages. These early events trigger a complex immune response that eventually involves many cellular subtypes of both innate and adaptive immunity. The Notch signaling pathway is an evolutionary conserved cell signaling system that mediates cell-to-cell communication. Recent studies have revealed that Notch modulate atherosclerosis by controlling macrophages polarization into M1 or M2 subtypes. Furthermore, it is known that Notch signaling controls differentiation and activity of T-helper and cytotoxic T-cells in inflammatory diseases. In this review, we will discuss the role of Notch in modulating immunity in the context of atherosclerosis and whether targeting Notch may represent a therapeutic strategy. atherosclerosis endothelial dysfunction Notch Dll4 immunity M1 macrophages Immunologic diseases. Allergy Francesca Fortini verfasserin aut Giorgio Aquila verfasserin aut Gianluca Campo verfasserin aut Gianluca Campo verfasserin aut Mauro Vaccarezza verfasserin aut Paola Rizzo verfasserin aut Paola Rizzo verfasserin aut Paola Rizzo verfasserin aut In Frontiers in Immunology Frontiers Media S.A., 2011 10(2019) (DE-627)657998354 (DE-600)2606827-8 16643224 nnns volume:10 year:2019 https://doi.org/10.3389/fimmu.2019.01130 kostenfrei https://doaj.org/article/3b9a37a3ff1b4953827d137964d408b9 kostenfrei https://www.frontiersin.org/article/10.3389/fimmu.2019.01130/full kostenfrei https://doaj.org/toc/1664-3224 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2019
language	English
source	In Frontiers in Immunology 10(2019) volume:10 year:2019
sourceStr	In Frontiers in Immunology 10(2019) volume:10 year:2019
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	atherosclerosis endothelial dysfunction Notch Dll4 immunity M1 macrophages Immunologic diseases. Allergy
isfreeaccess_bool	true
container_title	Frontiers in Immunology
authorswithroles_txt_mv	Francesco Vieceli Dalla Sega @@aut@@ Francesca Fortini @@aut@@ Giorgio Aquila @@aut@@ Gianluca Campo @@aut@@ Mauro Vaccarezza @@aut@@ Paola Rizzo @@aut@@
publishDateDaySort_date	2019-01-01T00:00:00Z
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callnumber-first	R - Medicine
author	Francesco Vieceli Dalla Sega
spellingShingle	Francesco Vieceli Dalla Sega misc RC581-607 misc atherosclerosis misc endothelial dysfunction misc Notch misc Dll4 misc immunity misc M1 macrophages misc Immunologic diseases. Allergy Notch Signaling Regulates Immune Responses in Atherosclerosis
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topic_title	RC581-607 Notch Signaling Regulates Immune Responses in Atherosclerosis atherosclerosis endothelial dysfunction Notch Dll4 immunity M1 macrophages
topic	misc RC581-607 misc atherosclerosis misc endothelial dysfunction misc Notch misc Dll4 misc immunity misc M1 macrophages misc Immunologic diseases. Allergy
topic_unstemmed	misc RC581-607 misc atherosclerosis misc endothelial dysfunction misc Notch misc Dll4 misc immunity misc M1 macrophages misc Immunologic diseases. Allergy
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title	Notch Signaling Regulates Immune Responses in Atherosclerosis
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title_full	Notch Signaling Regulates Immune Responses in Atherosclerosis
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title_sort	notch signaling regulates immune responses in atherosclerosis
callnumber	RC581-607
title_auth	Notch Signaling Regulates Immune Responses in Atherosclerosis
abstract	Atherosclerosis is a chronic autoimmune inflammatory disease that can cause coronary artery disease, stroke, peripheral artery disease, depending on which arteries are affected. At the beginning of atherosclerosis plasma lipoproteins accumulate in the sub-endothelial space. In response, monocytes migrate from the circulation through the endothelium into the intima where they differentiate into macrophages. These early events trigger a complex immune response that eventually involves many cellular subtypes of both innate and adaptive immunity. The Notch signaling pathway is an evolutionary conserved cell signaling system that mediates cell-to-cell communication. Recent studies have revealed that Notch modulate atherosclerosis by controlling macrophages polarization into M1 or M2 subtypes. Furthermore, it is known that Notch signaling controls differentiation and activity of T-helper and cytotoxic T-cells in inflammatory diseases. In this review, we will discuss the role of Notch in modulating immunity in the context of atherosclerosis and whether targeting Notch may represent a therapeutic strategy.
abstractGer	Atherosclerosis is a chronic autoimmune inflammatory disease that can cause coronary artery disease, stroke, peripheral artery disease, depending on which arteries are affected. At the beginning of atherosclerosis plasma lipoproteins accumulate in the sub-endothelial space. In response, monocytes migrate from the circulation through the endothelium into the intima where they differentiate into macrophages. These early events trigger a complex immune response that eventually involves many cellular subtypes of both innate and adaptive immunity. The Notch signaling pathway is an evolutionary conserved cell signaling system that mediates cell-to-cell communication. Recent studies have revealed that Notch modulate atherosclerosis by controlling macrophages polarization into M1 or M2 subtypes. Furthermore, it is known that Notch signaling controls differentiation and activity of T-helper and cytotoxic T-cells in inflammatory diseases. In this review, we will discuss the role of Notch in modulating immunity in the context of atherosclerosis and whether targeting Notch may represent a therapeutic strategy.
abstract_unstemmed	Atherosclerosis is a chronic autoimmune inflammatory disease that can cause coronary artery disease, stroke, peripheral artery disease, depending on which arteries are affected. At the beginning of atherosclerosis plasma lipoproteins accumulate in the sub-endothelial space. In response, monocytes migrate from the circulation through the endothelium into the intima where they differentiate into macrophages. These early events trigger a complex immune response that eventually involves many cellular subtypes of both innate and adaptive immunity. The Notch signaling pathway is an evolutionary conserved cell signaling system that mediates cell-to-cell communication. Recent studies have revealed that Notch modulate atherosclerosis by controlling macrophages polarization into M1 or M2 subtypes. Furthermore, it is known that Notch signaling controls differentiation and activity of T-helper and cytotoxic T-cells in inflammatory diseases. In this review, we will discuss the role of Notch in modulating immunity in the context of atherosclerosis and whether targeting Notch may represent a therapeutic strategy.
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title_short	Notch Signaling Regulates Immune Responses in Atherosclerosis
url	https://doi.org/10.3389/fimmu.2019.01130 https://doaj.org/article/3b9a37a3ff1b4953827d137964d408b9 https://www.frontiersin.org/article/10.3389/fimmu.2019.01130/full https://doaj.org/toc/1664-3224
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up_date	2024-07-03T14:17:49.542Z
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