Table 1 Summary of Th Cell Types: Classification, Surface Markers, Origins, and Functions.
Th cells classification | Surface marker | Function after MI | Origins |
|---|---|---|---|
Th1 | CD3,CD4,CD119,CD183(CXCR3),CD195(CCR5)… | Exacerbates the inflammatory response, leading to cardiomyocyte apoptosis and tissue damage, while also facilitating the process of cell debris removal [43]. Inhibited the production of reparative macrophages and enhanced the activity of other immune cells, contributed to the exacerbation of myocardial reperfusion injury [16]. Inhibition of cytokines such as TGF-β, IL-4, and IL-13 restricts fibroblast activation and collagen synthesis, thereby reducing fibrosis after myocardial infarction [56]. The concomitant production of IP-10 also has an antifibrotic effect [58]. | Naive T cells |
Th2 | CD3,CD4,CD119,CD193(CCR3),CD194(CCR4),CD365(Tim-1)… | Promotes myocardial tissue repair by modulating macrophage phenotype, inhibiting inflammatory cells and thereby suppressing excessive inflammatory response, and increasing proliferation of repair-related cells [79, 80]. Promoting fibrosis in injured myocardium may lead to pathological scarring and hyper fibrosis [82]. | Naive T cells |
Th9 | CD3,CD4,TCR α/β… | Complement cascade-induced reperfusion injury is associated with IL-9 [101]. Regulatory role in clinical I/R injury [102]. Enhancement of killing activity of CD8 + T cells to enhance inflammatory response and injury [99]. | Naive T cells |
Th17 | CD3,CD4,TCR α/β, IL-23R, CD194(CCR4),CD196(CCR6)… | Increased neutrophil infiltration promotes inflammatory response, exacerbates myocardial injury [122]. Causing cell death in Ly6Clow macrophages to slow the wound healing process leads to decreased survival after myocardial infarction [124]. Promoting matrix remodeling after myocardial injury by producing repair-related components such as MMPs or proteoglycans [128, 129]. | Naive T cells |
Th22 | CD3,CD4,TCR α/β,CD194(CCR6),CD196(CCR6),CCR10… | Inhibition of leukocyte accumulation and modulation of the inflammatory response leads to improved cardiac function after myocardial infarction [147]. Direct inhibition of myocardial apoptosis [150]. | Naive T cells |
Other:Th3 | CD3,CD4,CD69,LAP,CD122… | May inhibit excessive inflammatory response and reduce inflammatory damage to cardiac tissue. Promote tissue repair to reduce pathological changes after myocardial infarction [162]. | Naive T cells |
