Abstract
Type 2 immunity participates in the pathogeneses of helminth infection and allergic diseases. Emerging evidence indicates that the components of type 2 immunity are also involved in maintaining metabolic hemostasis and facilitating the healing process after tissue injury. Numerous preclinical studies have suggested regulation of type 2 immunity-related cytokines, such as interleukin-4, -13, and -33, and cell types, such as M2 macrophages, mast cells, and eosinophils, affects cardiac functions after myocardial infarction (MI), providing new insights into the importance of immune modulation in the infarcted heart. This review provides an overview of the functions of these cytokines and cells in the setting of MI as well as their potential to predict the severity and prognosis of MI.
Highlights
Type 2 immunity is characterized by the production of interleukin (IL)-4, IL-5, IL-9, IL-13, IL-25, IL-33, and thymic stromal lymphopoietin, as well as specific cell types including mast cells, eosinophils, basophils, alternatively activated M2 macrophages, type 2 innate lymphoid cells (ILC2), and T-helper (Th) 2 cells
Treatment of anti-IL-4 neutralizing antibodies reduces both the number and proliferation of fibroblasts as well as infiltration of CD68+ macrophages [7]. These findings suggest the sophisticated interaction between IL-4 and various cell types in the heart, which may lead to opposing outcomes under different pathological conditions
Modulation Methods and Polarization Mechanisms numerous methods have been applied to promote the shift from M1 macrophages toward M2 macrophages after myocardial infarction (MI), the precise mechanisms of M1/M2 polarization have not been fully investigated in most studies (Table 1)
Summary
Type 2 immunity is characterized by the production of interleukin (IL)-4, IL-5, IL-9, IL-13, IL-25, IL-33, and thymic stromal lymphopoietin, as well as specific cell types including mast cells, eosinophils, basophils, alternatively activated M2 macrophages, type 2 innate lymphoid cells (ILC2), and T-helper (Th) 2 cells. IL-33 treatment significantly suppresses proinflammatory cytokine and chemokine expression, including IL-1β, IL-6, IL-17, tumor necrosis factor-α (TNF-α), monocyte chemoattractant protein (MCP)-1, and interferon-γ (IFN-γ)-induced protein 10, and reduces macrophage infiltration after MI These effects are mediated by inhibition of p38 mitogen-activated protein kinase and nuclear factor kappa-light-chain-enhancer of activated B cells pathways [30]. Coculture with M2 macrophages isolated from the infarcted myocardium [86] or their secretome [87] enhances activation of cardiac fibroblasts in vitro These effects might be ascribed to IL-1α and osteopontin, because gene expression of Il1α and Spp is increased in M2 macrophages at 7 days after MI, and neutralization of IL-1α or osteopontin significantly reduces the fibroblastmyofibroblast transition when cocultured with M2 macrophages [86]. It has been confirmed that IL-4 and IL-13 mediate macrophage polarization toward M2a macrophages depending
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
