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Table 2 Summary table of differentiated allogeneic MSC in myocardial regeneration models

From: Changes in immunological profile of allogeneic mesenchymal stem cells after differentiation: should we be concerned?

Paper Model In vitro immunogenicity In vitro immunosuppressive ability In vivo engraftment In vivo immune marker expression In vivo functional benefits In vivo cellular response In vivo antibody response
Xia and Cao [47] Balb/C cardiomyocyte dMSCs to C57/BL6 mouse MI model Increased MHCI and MHCII expression on cardiomyocyte dMSCs NT Both undifferentiated and differentiated allogeneic MSCs engrafted. Over 4 weeks dMSCs were cleared quicker than undifferentiated NT Both differentiated and undifferentiated MSCs improved function at 2 weeks over controls; however, by 4 weeks benefit due to dMSCs was lost CD4+ and CD8+ infiltration in both undifferentiated and differentiated groups; significantly more in differentiated NT
Huang et al.[6] Wistar rat (allogeneic) or Lewis (syngeneic) MSCs to Lewis rat MI model MHCIa upregulated and MHCIb downregulated after in vitro differentiation. MHCII and CD86 co-expressed by dMSCs. Increased susceptibility to cytotoxic lysis NT Significantly more undifferentiated MSCs than dMSCs were engrafted at day 7 Engrafted dMSCs co-expressed MHCI or MHCII with differentiation markers Allogeneic MSC-treated animals displayed loss of functional benefit over time compared to syngeneic MSC-treated animals Leukocyte infiltration into allogeneic MSC-treated hearts Allo-antibodies produced against differentiated but not undifferentiated MSCs
Dhingra et al.[18] Wistar MSCs to Lewis rat MI dMSCs more susceptible to cytotoxic lysis MSCs lose ability to secrete PGE2 as they differentiate, which results in reduced ability to induce Tregs MSCs were eliminated by 5 weeks; some remained engrafted after PGE2 augmentation NT Improvement noted, but this was significantly less than if PGE2 was co-administered with allogeneic MSCs Increased CD8+ T-cell infiltration in dMSC-treated hearts, which could be rescued by PGE2 Allo-antibodies produced against dMSCs, which could be reduced by PGE2
Amado et al.[43] Allogeneic porcine MSCs to porcine MI NT NT Reported 42.4 ± 15% engraftment at 8 weeks. Labelled engrafted cells co-expressed differentiation markers NT Significant improvement after 8 weeks NT NT
Makkar et al.[44] Allogeneic porcine MSCs to porcine heart 1 month after MI NT NT Engrafted cells detected 2 months after injection NT No further deterioration in treated group compared to control NT NT
Perin et al.[45] Allogeneic canine MSCs to canine MI model delivered either intra-coronarily or transendocardially NT NT Engrafted cells detected 14 days after administration NT Transendocardially delivered allo-MSCs provided a functional benefit NT NT
Quevedo et al.[42] Allogeneic porcine MSCs to porcine MI NT NT Engrafted cells detected at 84 days co-expressing differentiation markers NT Improved cardiac function compared to control group NT NT
Dai et al.[46] Allogeneic ACI rat MSCs to Fischer rat MI NT NT 7 of 7 hearts at 6 months showed engrafted MSCs that co-expressed myocardium markers NT Improved LVEF at 4 weeks in allogeneic MSC-treated rats compared to control; effects were lost by 6 months NT NT
  1. Data related to immunological profile of MSCs both in vitro and in vivo are collated. dMSC, differentiated mesenchymal stem cell; LVEF, left ventricular ejection fraction; MHCI, major histocompatibility complex class I; MHCII, major histocompatibility class II; MI, myocardial infarction; MSC, mesenchymal stem cell; NT, not tested; PGE2, prostaglandin E2; Tregs, regulatory T cells.