Adaptive Immune Responses Contribute to Post-ischemic Cardiac Remodeling

Frontiers in Cardiovascular Medicine

Hafid Ait-Oufella¹  Icia Santos-Zas²  Alain Tedgui²  Jérémie Lemarié³ 

[1] AP-HP (Assistance Publique-Hôpitaux de Paris), Hôpital Saint-Antoine, Sorbonne Université, Paris, France;INSERM UMR-S 970, Sorbonne Paris Cité, Paris Cardiovascular Research Center – PARCC, Université Paris Descartes, Paris, France;UMR_S 1116, Université de Lorraine, Inserm, DCAC, Centre Hospitalier Régional Universitaire de Nancy – Réanimation Médicale – Hôpital Central, Nancy, France;

关键词: T lymphocytes;    B lymphocytes;    dendritic cells;    antibodies;    cardiovascular disease;    myocardial infarction;   

DOI  :  10.3389/fcvm.2018.00198

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown