ReviewCurrent opinion in neurology2022
Novel pathophysiological insights in autoimmune myasthenia gravis.
Review in Current opinion in neurology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Initiation response, maximized therapeutic efficacy, and post-treatment effects of biological targeted therapies in myasthenia gravis: a systematic review and network meta-analysis.Frontiers in neurology · 2024Pooled it
- HMGB1-mediated endoplasmic reticulum stress in monocyte-derived dendritic cells regulates CD4+ T cell immune responses in myasthenia gravis.Journal of neuroinflammation · 2026Article
- IgA autoantibodies demonstrate a novel mechanism of MuSK myasthenia gravis pathology.Brain : a journal of neurology · 2026Article
- DIA-based serum proteomics of the complement-coagulation cascade identifies candidate biomarkers for myasthenia gravis.Frontiers in neuroscience · 2026Article
- The immune microenvironment and population heterogeneity in myasthenia gravis: implications for precision therapeutics.Frontiers in immunology · 2026Review
- Circulating inflammatory cytokines and the risk of myasthenia gravis: a bidirectional Mendelian randomization study.BMC neurology · 2025Article
- Efgartigimod Followed by Telitacicept in Adult Generalized Myasthenia Gravis: A Retrospective Case Series.Journal of inflammation research · 2025Article
- Efgartigimod for generalized myasthenia gravis: A multicenter real-world cohort study in China.Annals of clinical and translational neurology · 2024Article
- Efgartigimod improves triple-negative myasthenia gravis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024Article
- Myasthenia gravis: the changing treatment landscape in the era of molecular therapies.Nature reviews. Neurology · 2024Review
- Independent risk factors for in-hospital outcome of myasthenic crisis: a prospective cohort study.Therapeutic advances in neurological disorders · 2024Article
- Complement biomarkers reflect the pathological status of neuromyelitis optica spectrum disorders.Frontiers in immunology · 2023Article
- Impact of Ravulizumab on Patient Outcomes and Quality of Life in Generalized Myasthenia Gravis.Patient related outcome measures · 2023Review
- Ravulizumab in Myasthenia Gravis: A Review of the Current Evidence.Neuropsychiatric disease and treatment · 2023Review
- Comparison of IVIg and TPE efficacy in the treatment of neurological disorders: a systematic literature review.Therapeutic advances in neurological disorders · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
purpose of reviewThis review summarizes recent insights into the immunopathogenesis of autoimmune myasthenia gravis (MG). Mechanistic understanding is presented according to MG disease subtypes and by leveraging the knowledge gained through the use of immunomodulating biological therapeutics. RECENT
findingsThe past two years of research on MG have led to a more accurate definition of the mechanisms through which muscle-specific tyrosine kinase (MuSK) autoantibodies induce pathology. Novel insights have also emerged from the collection of stronger evidence on the pathogenic capacity of low-density lipoprotein receptor-related protein 4 autoantibodies. Clinical observations have revealed a new MG phenotype triggered by cancer immunotherapy, but the underlying immunobiology remains undetermined. From a therapeutic perspective, MG patients can now benefit from a wider spectrum of treatment options. Such therapies have uncovered profound differences in clinical responses between and within the acetylcholine receptor and MuSK MG subtypes. Diverse mechanisms of immunopathology between the two subtypes, as well as qualitative nuances in the autoantibody repertoire of each patient, likely underpin the variability in therapeutic outcomes. Although predictive biomarkers of clinical response are lacking, these observations have ignited the development of assays that might assist clinicians in the choice of specific therapeutic strategies. SUMMARY: Recent advances in the understanding of autoantibody functionalities are bringing neuroimmunologists closer to a more detailed appreciation of the mechanisms that govern MG pathology. Future investigations on the immunological heterogeneity among MG patients will be key to developing effective, individually tailored therapies.
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What OpenQuestion holds
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.