Anti-inflammatory phenotypes of immune cells after myocardial infarction and prospects of therapeutic strategy.

Often causing negative cardiac remodeling and heart failure, a major threat to human life and health, myocardial infarction (MI) is a cardiovascular disease with a high morbidity and fatality rate worldwide. Maintaining ordinary heart function depends significantly on the immune system. Necrotic cardiomyocyte signals promote specific immunity and activate general immunity as the disease progresses in MI. Complex immune cells play a key role in all stages of MI progression by removing necrotic cardiomyocytes and tissue and promoting the healing of damaged tissue cells. Immune cells can help to regrow injured heart muscle as well as enable both inflammation and cardiomyocyte death. Immune cells are essential elements that help the immune system carry out its protective function. There are two types of immunity: nonspecific immunity and specific immunity. Developed throughout the long-term evolution of species, nonspecific immunity (including macrophages, myeloid-derived suppressor cells MDSC, natural killer cells NK, neutrophils, and dendritic cells DC) offers immediate and conservative host defense that might destroy healthy tissues because of its nonspecific nature. Precisely acquired immunity, specific immunity helps humoral and cellular immunity mediated through B and T cells correspondingly. These findings offer crucial information needed for the creation of effective immunomodulatory treatment, as discussed in this article.