Regulation of Type 2 Immunity in Myocardial Infarction

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.

Eosinophils improve cardiac function after myocardial infarction

“…Observations, such as the greatly reduced augmentation in IL4 in ΔdblGATA mice post MI, support this hypothesis. Yet, Th2 and NKT cells in post-MI hearts may also contribute to IL4 production in this context [47][48][49] . IL4 from these inflammatory cells may exert actions similar to that of IL4 from EOS in repairing heart from post-MI injury, a hypothesis that this study did not test.…”

Macrophage Polarization in Cardiac Tissue Repair Following Myocardial Infarction

“…Additionally, specific factors can cause M2 macrophages differentiation into four subtypes—M2a, M2b, M2c and M2d—each of which produces alternative sets of cytokines ( Figure 1 ). Specific factors include, but are not limited to, IL-4 or IL-13 for M2a, toll-like receptor (TLR) agonists or IL-1 receptor ligands for M2b, IL-10 or glucocorticoids for M2c and IL-6 or Toll-like receptor (TLR) agonists for M2d [ 42 , 43 ]. M2a macrophages, or wound healing M2, are characterized by an enhanced expression of CD206, CCL2, CCL17, CCL22 and CCL24 [ 43 ].…”

“…Specific factors include, but are not limited to, IL-4 or IL-13 for M2a, toll-like receptor (TLR) agonists or IL-1 receptor ligands for M2b, IL-10 or glucocorticoids for M2c and IL-6 or Toll-like receptor (TLR) agonists for M2d [ 42 , 43 ]. M2a macrophages, or wound healing M2, are characterized by an enhanced expression of CD206, CCL2, CCL17, CCL22 and CCL24 [ 43 ]. M2a macrophages play a significant role in ECM formation, as well as tissue repair and restoration, by secreting TGF-β, fibronectin, β IG-H3 and factor VIII subunit A. M2b macrophages are characterized by CCL1, tumor necrosis factor superfamily member 14 (TNFSF14) and CD86 markers [ 42 ].…”

Considering Cause and Effect of Immune Cell Aging on Cardiac Repair after Myocardial Infarction

“…Type 2 ILCs are a part of type 2 immunity which includes Th2 cells, M2 macrophages, eosinophils and mast cells. As a whole, the role of type 2 immunity on cardiac repair post-MI is unclear [78]. As the tools used to identify cell populations improve, our understanding of the role of lymphoid cells in cardiac disease is sure to grow and will undoubtedly lead to more questions.…”