Mesenchymal Stromal Cell-Based Immunotherapy for Type 1 Diabetes: From Bench to Bedside
- 1Institute of Biomedical Chemistry (IBMC), 119121 Moscow, Russia
- 2Endocrinology Research Centre, 117292 Moscow, Russia
Abstract
Type 1 diabetes mellitus (T1D) is an autoimmune disease characterized by the progressive destruction of pancreatic β-cells. Despite advances in glucose monitoring and insulin delivery, current treatments do not directly target the underlying autoimmune process. The administration of mesenchymal stromal cells (MSCs) represents a promising therapeutic approach due to their immunomodulatory, anti-inflammatory, and regenerative properties. Unlike therapies targeting individual immune pathways, MSCs exert broad immunomodulatory effects. This review integrates current knowledge of T1D immunopathogenesis with evidence on MSC-mediated immunomodulation, highlighting the ability of MSCs to modulate multiple interconnected mechanisms, including innate and adaptive immunity, antigen presentation, inflammatory signaling, and immune tolerance. Preclinical evidence suggests that MSCs may attenuate inflammation, regulate immune responses, preserve β-cell function, and improve metabolic outcomes. A preliminary but encouraging finding from clinical studies is that MSC administration may produce sustained beneficial effects after a limited number of injections. However, this observation remains tentative and requires confirmation in further studies. Standardized treatment protocols, adequately powered controlled trials, and long-term follow-up are needed to establish the clinical efficacy, durability of response, and optimal use of MSC-based therapy in T1D.
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BibTeX
@article{lupatov2026mesenchymal,
title = {{Mesenchymal Stromal Cell-Based Immunotherapy for Type 1 Diabetes: From Bench to Bedside}},
author = {Alexey Lupatov and Irina Pokusaeva and Irina Kholodenko and Marina Shestakova and Kirill Larin and Rita Khusainova and Ildar Minniakhmetov and Vladimir Chekhonin and Konstantin Yarygin and Natalia Mokrysheva},
journal = {International Journal of Molecular Sciences},
year = {2026},
month = nov,
doi = {10.3390/ijms272110005},
url = {https://www.mdpi.com/1422-0067/27/21/10005},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Mesenchymal Stromal Cell-Based Immunotherapy for Type 1 Diabetes: From Bench to Bedside
AU - Alexey Lupatov
AU - Irina Pokusaeva
AU - Irina Kholodenko
AU - Marina Shestakova
AU - Kirill Larin
AU - Rita Khusainova
AU - Ildar Minniakhmetov
AU - Vladimir Chekhonin
AU - Konstantin Yarygin
AU - Natalia Mokrysheva
PY - 2026
DA - 2026/11/08
JO - International Journal of Molecular Sciences
DO - 10.3390/ijms272110005
UR - https://www.mdpi.com/1422-0067/27/21/10005
AB - Type 1 diabetes mellitus (T1D) is an autoimmune disease characterized by the progressive destruction of pancreatic β-cells. Despite advances in glucose monitoring and insulin delivery, current treatments do not directly target the underlying autoimmune process. The administration of mesenchymal stromal cells (MSCs) represents a promising therapeutic approach due to their immunomodulatory, anti-inflammatory, and regenerative properties. Unlike therapies targeting individual immune pathways, MSCs exert broad immunomodulatory effects. This review integrates current knowledge of T1D immunopathogenesis with evidence on MSC-mediated immunomodulation, highlighting the ability of MSCs to modulate multiple interconnected mechanisms, including innate and adaptive immunity, antigen presentation, inflammatory signaling, and immune tolerance. Preclinical evidence suggests that MSCs may attenuate inflammation, regulate immune responses, preserve β-cell function, and improve metabolic outcomes. A preliminary but encouraging finding from clinical studies is that MSC administration may produce sustained beneficial effects after a limited number of injections. However, this observation remains tentative and requires confirmation in further studies. Standardized treatment protocols, adequately powered controlled trials, and long-term follow-up are needed to establish the clinical efficacy, durability of response, and optimal use of MSC-based therapy in T1D.
SN - 1422-0067
ER -