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Table 2 The pre-clinical results and clinical outcomes for each autoimmune disease with respect to PMSC types

From: The therapeutic applications of mesenchymal stromal cells from human perinatal tissues in autoimmune diseases

Type of autoimunne diseases Type of PMSCs Pre-clinical results References
 SLE UCMSCs Inhibiting B cell activity and autophagy activation in T cells; inducing CD4+ T cell apoptosis; upregulating the ratio of Th2/Th1; promoting generation of Treg cells, CD1c+DCs, and CD206+ M2 macrophages [24, 34, 38, 39, 47, 48, 51]
 LN UCMSCs Downregulating the levels of proteinuria, serum creatinine, anti-dsDNA antibody, IgG, and C3 deposition; inducing macrophages to M2 phenotype [56, 57]
PDMSCs Reducing the severity of proteinuria, production of anti-dsDNA antibodies; inhibiting the expression of inflammatory cytokines NF-κB, TNF-α, etc. [58]
 RA UCMSCs Decreasing the ratio of Th17/Treg cells; inhibiting the expression of CDH11; downregulating the levels of TNFα, IL-6, MCP-1, and IL-17, and upregulating the levels of IL-10 and TGF-β [62,63,64]
UCBMSCs Downregulating TNF-α, IL-1, and IFN-γ, but upregulating IL-10; reducing the infiltration of immune cells and hypertrophy of the synovial tissue [66, 68]
 EAE UCMSCs Ameliorating demyelination, axonal damage, and promoting remyelination in the spinal cord; modulating the ratio of Th1/Th2 cells and Th17/Treg cells in the spleen; increasing IL-4 and IL-10 but decreasing IL-1 and IL-6 in the spinal cord [71,72,73]
PDMSCs Decreasing infiltrating inflammatory cells, preserving axons, and ameliorating demyelination; decreasing the levels of COX-2, NF-kB, TNF-α, IFN-γ, and IL-2, and increasing production of IL-4 and TGF-β [77, 78, 80]
 Psoriasis UCMSCs Ameliorate the skin inflammation; attenuating plasmacytoid DCs to produce type I IFN [84]
UCBMSCs Downregulating IL-6, IL-17, TNF-α, CCL17, CCL20, and CCL27 [85]
AMSCs Decreasing both IL-17A and IL-22 production by cutaneous γδ-low T cells [86]
 Primary Sjögren’s syndrome UCMSCs Suppressing the T cell proliferation and restoring the Treg/Th17 ratio of PBMCs; downregulating the production of IFN-γ, IL-6, and TNFα but upregulating production of IL-10; suppressing the differentiation and proliferation of Tfh cells; inducing macrophages into an M2 phenotype [88, 90, 91, 95]
 T1D AFSCs Preserving and promoting endogenous β cell functionality and proliferation [97]
Type of autoimunne diseases Type of PMSCs Clinical outcomes References
 SLE UCMSCs Exhibiting a good safety profile in SLE patients; upregulating the ratio of Treg/Th17; 32.5% patients achieved major clinical response and 27.5% patients achieved partial clinical response during 12 months of follow-up. 12.5% and 16.7% patients experienced disease relapse at 9 months and 12 months [104, 105]
 LN UCMSCs Exhibiting a good safety profile in LN patients; ameliorating renal activity, renal function, glomerular filtration rate, and total disease activity [25, 106, 107]
 RA UCMSCs Exhibiting a good safety profile in RA patients; decreasing health index and joint function index of 1 year and 3 years after treatment; decreasing the serum levels of TNF-α and IL-6; increasing the percentage of Treg cells in peripheral blood [26, 109]
UCBMSCs Exhibiting a good safety profile in RA patients; reducing levels of IL-1β, IL-6, IL-8, and TNF-α; increasing the percentage of Treg cells in peripheral blood; reducing the mean 28-joint disease activity score at week 4 [108]
 MS PDMSCs Exhibiting a good safety profile in MS patients; decreasing Expanded Disability Status Scale scores [27]
 Psoriasis UCMSCs Reducing the severity and development of psoriasis at least 4 years [110]
 T1D UCMSCs Increasing levels of C peptide and decreasing HbA1c, fasting glycemia, and daily insulin requirements [28, 111]