Table 3.

Recent recognitions upon potential MIRI-related immunity.

Model	Effector	Target	Activity in MIRI	Ref.
Mouse	Tregs	Epicardial YAP/TAZ	The novel Hippo signaling effectors YAP/TAZ within epicardial can drive the immune chemokine target IFN-γ of Tregs to the injured myocardium and function as cardioprotectors post-AMI.	[93]
	CD39 of Tregs	Unknown	Attenuates cardiomyocyte apoptosis and reduces neutrophil infiltration.	[92]
	Key secreted proteins of Tregs	Unknown	Tregs function in a paracrine manner to promote cardiomyocyte proliferation for cardioprotection after AMI. The six secreted proteins including Cst7, Tnfsf11, Il33, Fgl2, Matn2, and Igf2 may be responsible.	[94]
	IL-2/Anti-IL-2 mAb complex (IL-2C)	Unknown	IL-2C from the spleen and heart might selectively proliferate cardioprotective Tregs.	[95]
	N,N-dimethylsphingosine (DMS)	IL-10, TGFβ	DMS applied during early AMI in vivo may be protective against MIRI by recruiting Tregs via the PI3K/Akt pathway.	[96]
	S1P/FTY720	CCL7, MMP-2 and IL-6	FTY720 can reduce immune B cells and its associated chemokine CCL7 and suppress MMP-2 and IL-6 in order to prevent the heart from severe cardiac inflammation and immune responses.	[102]
	TRAF3IP2 (previously known as CIKS or Act1)	NF-κB, JNK, p38 MAPK	Traf3ip2 gene deletion mediates an overall cardioprotective effects.	[104, 105]
	IL-21	Akt, NF-κB, p38MAPK	Increases chemokine expression by activating Akt/NF-κB signaling in cardiomyocytes and p38 MAPK/NF-κB signaling in cardiac fibroblasts.	[106]
	Crk adaptor proteins	C3G, RAP1	Crk adaptor proteins can mediate the initial steps of T-cells adhesion via its nSH3 domain binding to C3G, which is guanine-nucleotide exchange factors for the small GTPases RAP1.	[107]
Rat	S1P/FTY720	(GSK)-3β, mPTP components	S1P receptor agonist FTY720 can inhibit GSK-3β and regulate opening of mPTP to be cardioprotective.	[101]
Human	Vildagliptin	TGF-β1	Vildagliptin can recruit Tregs by overexpressing TGF-β1.	[97]