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Mesenchymal Stem Cells Suppress Dendritic Cells and Modulate Proinflammatory Milieu Through Interleukin-10 Expression in Peripheral Blood Mononuclear Cells of Human Systemic Lupus Erythematosus
BACKGROUND: Immune-mediated inflammatory injury among systemic lupus erythematosus (SLE) individuals may be involved by dendritic cells (DCs) abnormality though the underlying mechanism remains incompletely understood. OBJECTIVE: This study aimed to elaborate MSCs’ potential in suppressing abnormal...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Academy of Medical sciences
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10082662/ https://www.ncbi.nlm.nih.gov/pubmed/37038492 http://dx.doi.org/10.5455/aim.2023.31.20-25 |
Sumario: | BACKGROUND: Immune-mediated inflammatory injury among systemic lupus erythematosus (SLE) individuals may be involved by dendritic cells (DCs) abnormality though the underlying mechanism remains incompletely understood. OBJECTIVE: This study aimed to elaborate MSCs’ potential in suppressing abnormal DCs cell function on peripheral blood mononuclear cells (PBMCs) among SLE patients. METHODS: MSCs were isolated from human umbilical cord blood. On the other side, human PBMCs were isolated from 20 active SLE patients and 5 healthy controls. The PBMCs of SLE patients were divided into 5 groups: sham (Sh) and control (C) groups were treated with standard medium, and the treatment groups (T1, T2 and T3) was co-cultured with hUC-MSC at doses of 1:1, 1:25, and 1:50 (MSCs:PBMCs). The expression of CD11c in DCs was analyzed using flow cytometry, while the level of TNF-α, IFN-γ, IL-6 and IL-10 was analyzed using cytometric bead array (CBA). RESULTS: The MSCs significantly downregulates CD11c of dendritic cells in all treatment groups. MSCs also significantly suppress the level of TNF-α, IFN-γ, IL-6 and the significantly enhance IL-10 level in all treatment groups. CONCLUSION: Therefore, MSCs could suppress DCs through regulating the proinflammatory milieu in PBMCs of SLE patients. |
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