Table 2.

List of in vivo studies in which the therapeutic potential of the administration of hMSCs for the treatment of type I diabetes mellitus was evaluated and the results obtained.

References	Autoimmune disease	Source of hMSC	Variables	Experimental model	Clinical and laboratory effects	Mechanism proposed
(164)	Type I diabetes mellitus	Bone marrow	None	Mice	↓Disease onset ↓Insulitis in the pancreas	↑Tregs in the pancreas
(74)	Type I diabetes mellitus	Adipose tissue	Administration of adipose tissue-derived MSCs overexpressing betatrophin Administration of adipose tissue-derived MSCs alone	Mice	↓Hyperglycemia ↓Weight loss Effectiveness of adipose tissue-derived MSCs overexpressing betatrophin > Effectiveness of adipose tissue-derived MSCs alone	↑Islet proliferation ↑Ngn3 transcription factor ↑Pax6 transcription factor ↑Islet production of insulin ↑β-cells ratio ↑IL-4 ↑IL-10 ↑IL-13 ↓TNF-α ↓NADP-cytochrome P450 reductase ↑XIAP in the islets ↑Bcl-xL in the islets ↑Bcl-2 in the islets ↓Caspase-3 in the islets ↓Apoptotic cells
(75)	Type I diabetes mellitus	Umbilical cord stroma	None	Mice	↑Survival rates ↓Blood glucose ↑Serum insulin levels ↑Glucose tolerance ↑C-peptide ↓Insulitis	↓Th1 cells ↓Th17 cells ↑Tregs ↓Dendritic cells ↓IFN-γ in the serum ↓IL-1β in the serum ↓TNF-α in the serum ↓CCL2 in the serum ↓IL-17 in the serum ↑IL-4 in the serum ↑IL-10 in the serum ↑TGF-β1 ↑Intact islets ↑Insulin-producing cells devided from the differentiation of umbilical cord stroma-derived MSCs
(76)	Type I diabetes mellitus	Umbilical cord stroma	Administration of umbilical cord-derived MSCs before the onset of type I diabetes	Mice	↓Disease onset ↑Fasting C-peptide ↓Insulitis	↑CD4+CD25+Foxp3+ Tregs ↓IL-2 ↓IFN-γ ↓TNF- α ↑Islet β-cells
			Treatment of type I diabetes with umbilical cord-derived MSCs after the onset of the disease		↓Fasting plasma glucose ↓Fed blood glucose ↑Fasting C-peptide ↓Insulitis
(77)	Type I diabetes mellitus	Bone marrow	None	Mice	↓Hyperglycemia ↓Area under the glycemia curve ↓Fasting glycemia ↑Serum insulin	↑Islet β-cells function ↓CD3+ cells ↓Islet infiltration ↑Larger pancreatic islets ↓IL-2 in the pancreas ↓IFN-γ in the pancreas ↓IL-4 in the pancreas
(79)	Type I diabetes mellitus	Bone marrow	None	Mice	↓Hyperglycemia ↑Insulin production ↑Human insulin in mice ↑C-peptide production	↑Nestin ↑Pdx1 transcription factor ↑Ngn3 transcription factor ↑Pax4 transcription factor ↑NeuroD1 transcription factor ↑Nkx2.2 transcription factor ↑Nkx6.1 transcription factor ↑PCSK1 gene ↑Insulin gene ↑Glucagon gene ↑PCSK1 gene ↑PP gene
(80)	Type I diabetes mellitus	Bone marrow	None	Mice	↓Hyperglycemia ↑Insulin levels	↓Fas in human islets ↓MiR-375 in human islets ↓PBMC activation ↓PBMC proliferation ↓IL-2 ↓IFN-γ ↓IL-2 receptor ↑HGF ↑IL-10 ↑VEGF ↑PGE-2 ↑TGF-β ↑Treg function ↓Islet β-cells apoptosis ↑Islet β-cells function against inflammatory cytokines ↓Immune reaction against transplanted islets after humanization of mice
(78)	Type I diabetes mellitus	Umbilical cord stroma	None	Humans	↓Post-prandial plasma glucose ↓Hemoglobin HbA1c ↑Fasting C peptide ↑C-peptide/glucose ratio	↑Islet β-cells function

Both the methodology employed and the results obtained by each article are represented in this table. Ngn3, neurogenin-3; Pax4, paired box gene 4; Pax6, paired box gene 6; IL-13, interleukin 13; XIAP, X-linked inhibitor of apoptosis protein; Bcl-xL, B-cell lymphoma-extra large; Bcl-2, B-cell lymphoma 2; Pdx1, pancreatic and duodenal homeobox 1; NeuroD1, neurogenic differentiation 1; Nkx2.2, homeobox protein Nkx-2.2; Nkx6.1, homeobox protein Nkx-6.1; PCSK1, proprotein convertase 1; PP, protein phosphatase; Fas, first apoptosis signal receptor; PBMC, peripheral blood mononuclear cell.