ArticleRheumatology and immunology research2022
Olfactory Ecto-mesenchymal Stem Cell-derived Exosomes Ameliorate Murine Sjögren's Syndrome via Suppressing Tfh Cell Response.
Article in Rheumatology and immunology research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- Extracellular vesicles in dry eye disease and Sjögren's syndrome: A systematic review on their diagnostic and therapeutic role.Survey of ophthalmologyPooled it
- Evaluating the efficacy of stem cells in treating severe dry eye disease.World journal of stem cells · 2025Review
- A review of the roles of exosomes in salivary gland diseases with an emphasis on primary Sjögren's syndrome.Journal of dental sciences · 2025Review
- Mechanism and application of mesenchymal stem cells and their secreting extracellular vesicles in regulating CD4Biophysics reports · 2024Article
- Targeted Therapy for Severe Sjogren's Syndrome: A Focus on Mesenchymal Stem Cells.International journal of molecular sciences · 2024Review
- Emerging Role and Mechanism of Mesenchymal Stem Cells-Derived Extracellular Vesicles in Rheumatic Disease.Journal of inflammation research · 2024Review
Corrections and comments
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Authors and funding
11 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objectives: To investigate the effect of olfactory ecto-mesenchymal stem cell-derived exosomes (OE-MSC-Exos) on T follicular helper (Tfh) cell response and their implication in treating experimental Sjögrens syndrome (ESS). Methods: C57BL/6 mice were immunized with salivary glands (SG) proteins to induce ESS mouse model. OE-MSC-Exos were added to the Tfh cell polarization condition, and the proportion of Tfh cells was detected by FCM. The PD-L1 of OE-MSCs was silenced with small interfering RNA to extract siPD-L1-OE-MSC-Exos. Results: We found that transfer of OE-MSC-Exos markedly attenuated disease progression and reduced Tfh cell response in mice with ESS. In culture, OE-MSC-Exos potently inhibited the differentiation of Tfh cells from naïve T cells. Moreover, OE-MSC-Exos expressed high level of the ligand for the programmed cell death protein 1 (PD-L1), knocking down PD-L1 expression in OE-MSC-Exos significantly decreased their capacity to suppress Tfh cell differentiation in vitro. Consistently, transfer of OE-MSC-Exos with PD-L1 knockdown exhibited profoundly diminished therapeutic effect in ESS mice, accompanied with sustained Tfh cell response and high levels of autoantibody production. Conclusion: Our results suggest that OE-MSC-Exos may exert their therapeutic effect in ameliorating ESS progression via suppressing Tfh cell response in a PD-L1-dependent manner.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.