Atherosclerosis (ATS) is a multifactorial inflammatory disease representing the major cause of cardiovascular disease (ASCVD). Among ASCVD, carotid artery stenosis (CS) represent a serious health problem worldwide causing =10% of strokes. Immune response underlying ATS is complex and is characterized by the activation of both innate and adaptive immune responses. In this review article has been revised the contribution of the main cell populations and mediators involved in ATS. Monocytes play a central role in atherogenesis by their ability to differentiate into macrophages, thus leading to lipid accumulation and foam cells formation. T lymphocytes are present into the atherosclerotic plaque, where, in response to the local milieu of cytokines, differentiate into different subpopulations. The role of B cells in ATS is still under evaluation, due also to B cell heterogeneity. Mast cells, by release of their contents, may actively contribute to atherosclerotic plaque progression and destabilization. Matrix metalloproteinases and cytokines are also involved in atherosclerotic process. Mechanisms underlying CS are complex and are influenced by inflammatory immune response occurring during ATS. Thus, beside information coming from neuroimaging and laboratory data, the knowledge of immunologic mechanisms could contribute to improve treatment decisions for these patients.

Inflammation and immune response in carotid artery stenosis / Del Porto, F; Cifani, N; Proietta, M; Dezi, T; Panzera, C; Ficarelli, R; Taurino, M. - In: ITALIAN JOURNAL OF VASCULAR AND ENDOVASCULAR SURGERY. - ISSN 1824-4777. - 26:1(2019), pp. 39-47. [10.23736/S1824-4777.18.01385-2]

Inflammation and immune response in carotid artery stenosis

Del Porto F
;
Cifani N;Proietta M;Dezi T;Panzera C;Ficarelli R;Taurino M
2019

Abstract

Atherosclerosis (ATS) is a multifactorial inflammatory disease representing the major cause of cardiovascular disease (ASCVD). Among ASCVD, carotid artery stenosis (CS) represent a serious health problem worldwide causing =10% of strokes. Immune response underlying ATS is complex and is characterized by the activation of both innate and adaptive immune responses. In this review article has been revised the contribution of the main cell populations and mediators involved in ATS. Monocytes play a central role in atherogenesis by their ability to differentiate into macrophages, thus leading to lipid accumulation and foam cells formation. T lymphocytes are present into the atherosclerotic plaque, where, in response to the local milieu of cytokines, differentiate into different subpopulations. The role of B cells in ATS is still under evaluation, due also to B cell heterogeneity. Mast cells, by release of their contents, may actively contribute to atherosclerotic plaque progression and destabilization. Matrix metalloproteinases and cytokines are also involved in atherosclerotic process. Mechanisms underlying CS are complex and are influenced by inflammatory immune response occurring during ATS. Thus, beside information coming from neuroimaging and laboratory data, the knowledge of immunologic mechanisms could contribute to improve treatment decisions for these patients.
2019
atherosclerosis; t-lymphocytes; regulatory; atherosclerotic lesions
01 Pubblicazione su rivista::01g Articolo di rassegna (Review)
Inflammation and immune response in carotid artery stenosis / Del Porto, F; Cifani, N; Proietta, M; Dezi, T; Panzera, C; Ficarelli, R; Taurino, M. - In: ITALIAN JOURNAL OF VASCULAR AND ENDOVASCULAR SURGERY. - ISSN 1824-4777. - 26:1(2019), pp. 39-47. [10.23736/S1824-4777.18.01385-2]
File allegati a questo prodotto
File Dimensione Formato  
DelPorto_Inflammation_2019.pdf

solo gestori archivio

Tipologia: Versione editoriale (versione pubblicata con il layout dell'editore)
Licenza: Tutti i diritti riservati (All rights reserved)
Dimensione 825.83 kB
Formato Adobe PDF
825.83 kB Adobe PDF   Contatta l'autore

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1278002
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus 0
  • ???jsp.display-item.citation.isi??? 0
social impact