ArticleJournal of neuroinflammation2020
Decreased expression of miR-29 family associated with autoimmune myasthenia gravis.
Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Jianpi Yiqi Busui prescription alleviates myasthenia gravis by regulating Th17 through the TAK1/P38 MAPK/eIF-4E signaling pathway.Biomolecules & biomedicine · 2025Article
- Optimization of Induction Protocols for Experimental Autoimmune Myasthenia Gravis.International journal of molecular sciences · 2025Article
- Development of a refined experimental mouse model of myasthenia gravis with anti-acetylcholine receptor antibodies.Frontiers in immunology · 2025Article
- Thyroid dysfunction in Hashimoto's thyroiditis: a pilot study on the putative role of miR-29a and TGFβ1.Endocrine · 2024Article
- The intricate dance of non-coding RNAs in myasthenia gravis pathogenesis and treatment.Frontiers in immunology · 2024Review
- Advancements and prospects of novel biologicals for myasthenia gravis: toward personalized treatment based on autoantibody specificities.Frontiers in pharmacology · 2024Review
- Myasthenia Gravis: Novel Findings and Perspectives on Traditional to Regenerative Therapeutic Interventions.Aging and disease · 2023Article
- miR-29a-3p promotes the regulatory role of eicosapentaenoic acid in the NLRP3 inflammasome and autophagy in microglial cells.The Kaohsiung journal of medical sciences · 2023Article
- Article
- MiR-29a-3p negatively regulates circulating Tfh memory cells in patients with Graves' disease by targeting ICOS.Immunologic research · 2023Article
- Circulating miRNA-19b as a biomarker of disease progression and treatment response to baricitinib in rheumatoid arthritis patients through miRNA profiling of monocytes.Frontiers in immunology · 2023Article
- Myasthenia Gravis: An Acquired Interferonopathy?Cells · 2022Review
- Regulatory roles of MicroRNA in shaping T cell function, differentiation and polarization.Seminars in cell & developmental biology · 2022Review
- DCAF12 and HSPA1A May Serve as Potential Diagnostic Biomarkers for Myasthenia Gravis.BioMed research international · 2022Article
- Practical Management for Use of Eculizumab in the Treatment of Severe, Refractory, Non-Thymomatous, AChR + Generalized Myasthenia Gravis: A Systematic Review.Therapeutics and clinical risk management · 2022Review
- A Review on the Role of Non-Coding RNAs in the Pathogenesis of Myasthenia Gravis.International journal of molecular sciences · 2021Review
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
backgroundMyasthenia gravis (MG) is a rare autoimmune disease mainly mediated by autoantibodies against the acetylcholine receptor (AChR) at the neuromuscular junction. The thymus is the effector organ, and its removal alleviates the symptoms of the disease. In the early-onset form of MG, the thymus displays functional and morphological abnormalities such as B cell infiltration leading to follicular hyperplasia, and the production of AChR antibodies. Type-I interferon (IFN-I), especially IFN-β, is the orchestrator of thymic changes observed in MG. As Dicer and miR-29 subtypes play a role in modulating the IFN-I signalization in mouse thymus, we investigated their expression in MG thymus.
methodsThe expression of DICER and miR-29 subtypes were thoroughly investigated by RT-PCR in human control and MG thymuses, and in thymic epithelial cells (TECs). Using miR-29a/b-1-deficient mice, with lower miR-29a/b-1 expression, we investigated their susceptibility to experimental autoimmune MG (EAMG) as compared to wild-type mice.
resultsDICER mRNA and all miR-29 subtypes were down-regulated in the thymus of MG patients and DICER expression was correlated with the lower expression of miR-29a-3p. A decreased expression of miR-29 subtypes was similarly observed in MG TECs; a decrease also induced in TECs upon IFN-β treatment. We demonstrated that miR-29a/b-1-deficient mice were more susceptible to EAMG without higher levels of anti-AChR IgG subtypes. In the thymus, if no B cell infiltration was observed, an increased expression of Ifn-β associated with Baff expression and the differentiation of Th17 cells associated with increased expression of Il-6, Il-17a and Il-21 and decreased Tgf-β1 mRNA were demonstrated in miR-29a/b-1-deficient EAMG mice.
conclusionsIt is not clear if the decreased expression of miR-29 subtypes in human MG is a consequence or a causative factor of thymic inflammation. However, our results from the EAMG mouse model indicated that a reduction in miR-29a/b1 may contribute to the pathophysiological process involved in MG by favoring the increased expression of IFN-β and the emergence of pro-inflammatory Th17 cells.
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