ArticleFrontiers in immunology2024
Exhausted signature and regulatory network of NK cells in myasthenia gravis.
Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Sinomenine ameliorates experimental autoimmune neuritis by suppressing pro-inflammatory immune components and restoring immune balance.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Article
- An Immune Model Incorporating NK Cells and IL-12 to Predict the Efficacy of the Initial Treatment Cycle of Efgartigimod in Generalized Myasthenia Gravis.Drug design, development and therapy · 2026Observational
- Targeting NF-kappaB-inducing kinase shapes B-cell homeostasis in myasthenia gravis.Journal of neuroinflammation · 2025Article
- A pilot study of the immunological profile and efficacy of rituximab in muscle-specific kinase antibody-positive myasthenia gravis.Frontiers in immunology · 2025Article
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Authors and funding
8 authors.
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Abstract
Introduction: NK cells are dysfunctional in myasthenia gravis (MG), but the mechanism is unclear. This study aims to measure associations and underlying mechanisms between the NK cells and the development of MG. Methods: Twenty healthy controls (HCs) and 53 MG patients who did not receive glucocorticoids and immunosuppressants were collected. According to the Myasthenia Gravis Foundation of America (MGFA) classification, MG patients were categorized into MGFA I group (n = 18) and MGFA II-IV group (n = 35). Flow cytometry, cell sorting, ELISA, mRNA-sequencing, RT-qPCR, western blot, and cell culture experiments were performed to evaluate the regulatory mechanism of exhausted NK cells. Results: Peripheral NK cells in MGFA II-IV patients exhibit exhausted phenotypes than HCs, marked by the dramatic loss of total NK cells, CD56 Discussion: Inhibition of IL-6/IL-21/SOCS2/STAT5 pathway and recovery of NK-cell ability to inhibit autoimmunity may be a new direction in the treatment of MG.
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