Table 1:

Summary of T-cell subsets involved in myocardial infarction (MI).

T-cell classification	Secretion profile	Function
Th1	Cxcl10, Ifnγ, IL-2, Tnfβ	Inhibit fibroblast proliferation, decrease expression of collagen-I and -III [24–26] Inhibit bFGF-induced fibroblast migration and wound contraction [27, 28] Indirectly regulate fibrosis through activation of macrophages [29, 30]
Th2	IL-4, IL-5, IL-6, IL-9, IL-10, IL-13,	Negatively regulate production of pro-inflammatory cytokines in macrophages [31–33]
Th17	IL-17, IL-21, IL-22, Ccl20	Indirectly regulate fibrosis through recruitment of neutrophils and macrophages [34, 35]
Treg	Tgfβ, IL-10	Secrete pro-fibrotic molecule TGF-0 [36, 37] Inhibit Th17-mediated fibrosis through IL-10 [36, 37] Direct contact stimulates fibroblast, decreases MMP-3, and preserves the matrix [38] Induce an M2-like macrophage differentiation [21, 38]
Cytotoxic	Performin, Granzyme B	Decrease cardiac rupture and increases collagen cross-linking [21] Decrease wound-breaking strength and collagen synthesis [39] Increase myofibroblast [21] Activate macrophage-mediated phagocytosis [21]

bFGF- basic fibroblast growth factor; IFN-interferon; IL-interleukin; MCP- monocyte chemotactic protein; TGF-transforming growth factor; TNF-tumor necrosis factor