Table 2.

Regulatory or reparative DAMPs and related molecules in Tx.

Family	Molecule	Receptors	Role in Tx- related inflammation/immunity/outcomes	References
Regulatory or reparative DAMPs
	CD24	Siglec	Associates with DAMPS to negatively regulate their stimulatory activity Protect against pathological inflammatory responses arising from cell death and necrosis Limits T cell alloimmunity	(70–73)
	IL-33	ST2	Promotes the systemic expansion of ST2+ Treg able to limit alloimmunity Promotes the secretion of Areg and other growth factors act on tissues and stem cells to support repair Induces TCR-independent Treg secretion of IL-13 and Areg that to control local inflammation and the generation of reparative type macrophages Directly promotes the generation of reparative macrophage phenotype through a metabolic reprogramming that augments OXHPOS and FA uptake	(74–82)
	Heat Shock Proteins (HSPs)	CD91, TLR2, TLR4, SREC1, and FEEL1	Supports debris clearance and wound repair Protect organs from IRI Extend graft survival Induce IL-10 secretion by T cells Support polarization of macrophages towards regulatory and reparative subsets	(24, 83–89)
	Hyaluronan	Lyve1	High weight forms support the survival and localization of macrophage subsets that productively remodel ECM to support vasculature function after injury Contribute to tissue integrity and functional immunological niches	(23, 90–94)
Specialized pro-resolving mediators (SPMs) and related molecules
	Annexin A1	FPR2/ALX	Polarization of macrophage towards a pro-reparative subset Prolong allografts survival with sub-therapeutic immunosuppression Protect organs after IRI	(95–99)
	Maresins, Lipoxins, and Resolvins	GPR32 and ALX/FPR2 receptors	Limiting neutrophil infiltration and induction of neutrophil apoptosis Directly limiting adaptive immune responses Organ-protective and regenerative actions after IRI Stimulate macrophage transition toward reparative subsets Enhance Treg functions Prolongation of allograft survival	(100–109)