Adaptive Immune Responses Contribute to Post-ischemic Cardiac Remodeling
Myocardial infarction (MI) is a common condition responsible for mortality and morbidity related to ischemic heart failure. Accumulating experimental and translational evidence support a crucial role for innate immunity in heart failure and adverse heart remodeling following MI. More recently, the r...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2019-01-01
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| Series: | Frontiers in Cardiovascular Medicine |
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| Online Access: | https://www.frontiersin.org/article/10.3389/fcvm.2018.00198/full |
| _version_ | 1819170608292823040 |
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| author | Icia Santos-Zas Jérémie Lemarié Jérémie Lemarié Alain Tedgui Hafid Ait-Oufella Hafid Ait-Oufella |
| author_facet | Icia Santos-Zas Jérémie Lemarié Jérémie Lemarié Alain Tedgui Hafid Ait-Oufella Hafid Ait-Oufella |
| author_sort | Icia Santos-Zas |
| collection | DOAJ |
| description | Myocardial infarction (MI) is a common condition responsible for mortality and morbidity related to ischemic heart failure. Accumulating experimental and translational evidence support a crucial role for innate immunity in heart failure and adverse heart remodeling following MI. More recently, the role of adaptive immunity in myocardial ischemia has been identified, mainly in rodents models of both transient and permanent heart ischemia. The present review summarizes the experimental evidence regarding the role of lymphocytes and dendritic cells in myocardial remodeling following coronary artery occlusion. Th1 and potentially Th17 CD4+ T cell responses promote adverse heart remodeling, whereas regulatory T cells appear to be protective, modulating macrophage activity, cardiomyocyte survival, and fibroblast phenotype. The role of CD8+ T cells in this setting remains unknown. B cells contribute to adverse cardiac remodeling through the modulation of monocyte trafficking, and potentially the production of tissue-specific antibodies. Yet, further substantial efforts are still required to confirm experimental data in human MI before developing new therapeutic strategies targeting the adaptive immune system in ischemic cardiac diseases. |
| first_indexed | 2024-12-22T19:38:06Z |
| format | Article |
| id | doaj.art-bf94231699ef4fa483c61a4e469282fc |
| institution | Directory Open Access Journal |
| issn | 2297-055X |
| language | English |
| last_indexed | 2024-12-22T19:38:06Z |
| publishDate | 2019-01-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Cardiovascular Medicine |
| spelling | doaj.art-bf94231699ef4fa483c61a4e469282fc2022-12-21T18:14:56ZengFrontiers Media S.A.Frontiers in Cardiovascular Medicine2297-055X2019-01-01510.3389/fcvm.2018.00198429788Adaptive Immune Responses Contribute to Post-ischemic Cardiac RemodelingIcia Santos-Zas0Jérémie Lemarié1Jérémie Lemarié2Alain Tedgui3Hafid Ait-Oufella4Hafid Ait-Oufella5INSERM UMR-S 970, Sorbonne Paris Cité, Paris Cardiovascular Research Center – PARCC, Université Paris Descartes, Paris, FranceINSERM UMR-S 970, Sorbonne Paris Cité, Paris Cardiovascular Research Center – PARCC, Université Paris Descartes, Paris, FranceUMR_S 1116, Université de Lorraine, Inserm, DCAC, Centre Hospitalier Régional Universitaire de Nancy – Réanimation Médicale – Hôpital Central, Nancy, FranceINSERM UMR-S 970, Sorbonne Paris Cité, Paris Cardiovascular Research Center – PARCC, Université Paris Descartes, Paris, FranceINSERM UMR-S 970, Sorbonne Paris Cité, Paris Cardiovascular Research Center – PARCC, Université Paris Descartes, Paris, FranceAP-HP (Assistance Publique-Hôpitaux de Paris), Hôpital Saint-Antoine, Sorbonne Université, Paris, FranceMyocardial infarction (MI) is a common condition responsible for mortality and morbidity related to ischemic heart failure. Accumulating experimental and translational evidence support a crucial role for innate immunity in heart failure and adverse heart remodeling following MI. More recently, the role of adaptive immunity in myocardial ischemia has been identified, mainly in rodents models of both transient and permanent heart ischemia. The present review summarizes the experimental evidence regarding the role of lymphocytes and dendritic cells in myocardial remodeling following coronary artery occlusion. Th1 and potentially Th17 CD4+ T cell responses promote adverse heart remodeling, whereas regulatory T cells appear to be protective, modulating macrophage activity, cardiomyocyte survival, and fibroblast phenotype. The role of CD8+ T cells in this setting remains unknown. B cells contribute to adverse cardiac remodeling through the modulation of monocyte trafficking, and potentially the production of tissue-specific antibodies. Yet, further substantial efforts are still required to confirm experimental data in human MI before developing new therapeutic strategies targeting the adaptive immune system in ischemic cardiac diseases.https://www.frontiersin.org/article/10.3389/fcvm.2018.00198/fullT lymphocytesB lymphocytesdendritic cellsantibodiescardiovascular diseasemyocardial infarction |
| spellingShingle | Icia Santos-Zas Jérémie Lemarié Jérémie Lemarié Alain Tedgui Hafid Ait-Oufella Hafid Ait-Oufella Adaptive Immune Responses Contribute to Post-ischemic Cardiac Remodeling Frontiers in Cardiovascular Medicine T lymphocytes B lymphocytes dendritic cells antibodies cardiovascular disease myocardial infarction |
| title | Adaptive Immune Responses Contribute to Post-ischemic Cardiac Remodeling |
| title_full | Adaptive Immune Responses Contribute to Post-ischemic Cardiac Remodeling |
| title_fullStr | Adaptive Immune Responses Contribute to Post-ischemic Cardiac Remodeling |
| title_full_unstemmed | Adaptive Immune Responses Contribute to Post-ischemic Cardiac Remodeling |
| title_short | Adaptive Immune Responses Contribute to Post-ischemic Cardiac Remodeling |
| title_sort | adaptive immune responses contribute to post ischemic cardiac remodeling |
| topic | T lymphocytes B lymphocytes dendritic cells antibodies cardiovascular disease myocardial infarction |
| url | https://www.frontiersin.org/article/10.3389/fcvm.2018.00198/full |
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