Myasthenia gravis (MG) is a chronic autoimmune disorder characterized by an immune-mediated attack on neuromuscular junction acetylcholine receptors (AChRs), and its pathogenesis is closely linked to immune dysregulation. Emerging evidence has highlighted the pivotal role of the gut microbiota in the pathophysiology of MG through immunomodulation, microbial metabolite signaling, and gut-brain axis interactions. This review combines 16S rRNA sequencing, metagenomic, and metabolomic data to reveal distinct gut microbial signatures in patients with MG. These signatures include reduced α-diversity, depletion of beneficial taxa like Bacteroides and Bifidobacterium, enrichment of pathobionts such as Escherichia and Enterococcus, and diminished levels of the short-chain fatty acids (SCFA), which were inversely correlated with disease severity. Experimental models have demonstrated that fecal microbiota transplantation (FMT) and probiotic supplementation with strains like Bifidobacterium ameliorate symptoms by restoring Th17/Treg equilibrium, suppressing the expression of pro-inflammatory cytokines including IL-6 and TNF-α, and enhancing intestinal barrier integrity. Mechanistically, gut dysbiosis exacerbates autoimmunity via NF-αB pathway activation, disrupts tryptophan metabolism and impairs gut-brain signaling. While existing studies have established microbiota-MG associations, further causal validation, personalized therapeutic strategies, and multi-omics integration remain critical priorities. Microbiota-targeted interventions, including precision FMT and metabolite delivery, hold translational potential, but their validation via large-scale randomized controlled trials and interdisciplinary approaches like AI-driven microbiota profiling is essential if they are to advance precision medicine for MG management.

Anti-MuSK antibody–positive myasthenia gravis (MuSK-MG) is characterized by severe and potentially life-threatening weakness. Anti-MuSK antibodies are key pathogenic drivers of this disorder. This review provides a comprehensive summary of the current state-of-the-art with respect to the understanding of MuSK and its role in MuSK-MG. MuSK, a receptor tyrosine kinase, is essential at the neuromuscular junction, where it forms an agrin–LRP4–MuSK tripartite functional complex that initiates and maintains agrin-induced acetylcholine receptor clustering at the postsynaptic membrane. Although anti-MuSK antibodies encompass all IgG subclasses (IgG1–4), IgG4 is the predominant pathogenic subclass. In vivo, IgG4 antibodies undergo Fab-arm exchange, acquiring functional monovalency; this monovalent IgG4 disrupts LRP4–MuSK interactions, thereby blocking downstream signaling and precipitating myasthenic symptoms. Emerging evidence indicates that IgG1–3 anti-MuSK antibodies are also pathogenic, although some clones exhibit agonistic effects on MuSK phosphorylation. Further, this review examines the various diagnostic methods for this condition and weighs the advantages and disadvantages. Both MuSK protein and its autoantibodies are pivotal for diagnosis and therapy. Radioimmunoprecipitation assays and enzyme-linked immunosorbent assays and their benefits ad limitations are discussed, and cell-based assays are noted for their high accuracy. Anti-MuSK antibody testing is the gold standard diagnostic biomarker. Finally, the review covers the various therapeutic strategies for MuSK-MG, including immunosuppressants, monoclonal antibodies, CAR-T cell therapy, and neonatal Fc receptor blockade. B-cell–targeted therapies (e.g., anti-CD20 monoclonal antibodies) and MuSK agonists represent promising future therapeutic strategies for MuSK-MG. Overall, this review provides a definitive summary of the present practices and future strategies for the diagnosis and treatment of MuSK-MG, laying out clear markers for further studies that have to be undertaken to enhance our understanding of this condition.

BACKGROUND:Anti-complex nucleosomal remodelling histone deacetylase (Mi2)-positive dermatomyositis (DM) is characterized by severe muscle damage. This study investigated muscle magnetic resonance imaging (MRI) features in anti-Mi2-positive DM, compared them with other DM subtypes, and evaluated their associations with clinical features. METHODS:DM patients who underwent thigh MRI were enrolled, including 20 anti-Mi2-positive, 20 anti-TIF1γ-positive, 15 anti-NXP2-positive, and 19 anti-MDA5-positive cases. Clinical and imaging data were collected and compared across subtypes. The relationship between MRI features and clinical characteristics was analysed in the anti-Mi2-positive subgroup. RESULTS:Among the four subtypes, anti-Mi2-positive DM had the highest myofascial oedema frequency in the sartorius and the lowest in the biceps femoris (both p < 0.05). All anti-Mi2-positive patients had muscle oedema - most severe in the quadriceps femoris with relative sparing of the semimembranosus and biceps femoris - and the highest total muscle oedema scores (p < 0.001). Eleven (55%) patients had fatty infiltration, predominantly in the gluteus maximus and hamstrings with sparing of the rectus femoris and adductor longus. In this subgroup, treatment-naïve patients had a higher prevalence of diffuse distribution than treatment-experienced (p = 0.042). Compared with anti-TIF1γ-positive patients, the anti-Mi2-positive subgroup had lower total fatty infiltration scores and milder gluteus maximus, adductor longus, and hamstrings involvement (all p < 0.05). In anti-Mi2-positive DM, total muscle oedema scores correlated negatively with Manual Muscle Testing-8 scores and positively with serum creatine kinase levels (both p < 0.05). Preliminary observations in six anti-Mi2-positive patients followed longitudinally showed that muscle oedema decreased after treatment, resolved during remission, and recurred with relapse. CONCLUSION:This study delineated baseline thigh MRI patterns in anti-Mi2-positive DM and demonstrated that baseline muscle oedema severity correlated with serological and clinical indicators of muscle damage. Additionally, findings from a small longitudinal cohort suggested a potential role for thigh MRI in assessing and monitoring muscle disease activity in this subtype, although these results are preliminary and require validation in larger studies.

Background Myasthenia gravis (MG) is one of the most prevalent disorder of the neuromuscular junction (NMJ). Non-coding RNAs regulate myoblast proliferation and differentiation. Methods The differential expression of miRNAs was analysed by using RNA microarrays. Protein levels and gene expression were analysed by using Western blotting and quantitative real-time polymerase chain reaction. The interactions of miR-4310 with circ_0018483 or ERBB receptor feedback inhibitor 1 (ERRFI1) were assessed using dual-luciferase reporter assays. The expression and aggregation of acetylcholine receptors (AChRs) were observed and analysed by using immunofluorescence. Results The expression of miR-4310 was downregulated in the whole blood of patients. circ_0018483 exhibited a sponge effect on miR-4310, and the inhibition of miR-4310 weakened AChR function. Additionally, miR-4310 targeted ERRFI1 and circ_0018483, and circ_0018483 affected the expression and aggregation of AChR by regulating miR-4310 and ERRFI1. circ_0018483 regulates the expression of ERRFI1 by targeting miR-4310, which in turn affects AChR expression and aggregation at the NMJ. Conclusions We confirmed a novel circ_0018483/miR-4310/ERRFI1 ceRNA axis in MG. Our findings suggest novel AChR regulation and MG molecular mechanisms research avenues.

Myasthenia gravis (MG) is a chronic, fluctuating neuromuscular disease characterised by fatigue. Patients with MG often suffer from mental stress and are prone to chronic stress responses (CSR), such as depression and anxiety. Although CSR can exacerbate MG symptoms, the precise mechanisms driving this aggravation are yet to be elucidated. In this study, we used experimental models of autoimmune MG (EAMG) and chronic unpredictable mild stress. We explored the possible mechanisms by which CSR aggravates MG symptoms and inhibits the activity of the hypothalamic-pituitary-adrenal (HPA) axis by studying the behaviour, immune function, and symptoms of experimental mice. We observed that CSR aggravated the symptoms of myasthenia in EAMG mice by enhancing the HPA axis activity and causing the inflammatory balance to shift in a proinflammatory direction. RU486, a glucocorticoid receptor antagonist, can alleviate the aggravation of CSR-induced MG symptoms by inhibiting the HPA axis activity, suggesting that the HPA axis is an important target for the treatment of CSR-related MG. This study provides a new explanation of the mechanism by which CSR aggravates MG symptoms.

BackgroundMyasthenia gravis (MG) is an autoimmune disorder mediated by autoantibodies. While research regarding the microbiota-gut-brain axis has expanded significantly in recent years, the role of the oral microbiota in MG and its potential association with systemic metabolism remain poorly understood. To address this, we conducted a case-control study to investigate potential alterations in the oral microbiota and serum metabolites in newly diagnosed and treatment-naïve patients with MG.MethodsIn total, 38 newly diagnosed and treatment-naïve anti-AchR antibody-positive MG patients were recruited, including 19 with ocular myasthenia gravis (OMG) and 19 with generalized myasthenia gravis (GMG), along with 29 healthy controls (HCs). Saliva and serum samples were collected for 16S rRNA gene high-throughput sequencing and untargeted metabolomic profiling, respectively. Data processing and integration were performed using multiple bioinformatics and statistical methods, including α- and β-diversity analyses, LEfSe, Spearman correlation, and metabolic pathway enrichment analysis.ResultsCompared with HCs, patients with OMG and GMG exhibited significant dysbiosis. At the phylum level, the abundance of Bacillota was significantly increased, whereas that of Bacteroidota and Campylobacterota was significantly decreased. At the genus level, the abundances of Streptococcus and Bifidobacterium were significantly elevated; in contrast, those of Prevotella and others were significantly reduced. Serum metabolomics analysis identified distinct metabolic disorders in MG patients, involving key pathways such as lipid metabolism, neuroactive ligand-receptor interaction, and amino acid metabolism. Correlation network analysis further revealed significant associations between specific oral genera (Streptococcus, Bifidobacterium) and differential metabolites primarily involved in lipid metabolism, amino acid metabolism, and terpenoid and polyketide metabolism in both OMG and GMG populations.ConclusionsIn MG patients, significant oral dysbiosis may be associated with MG-related metabolic alterations by disrupting metabolic pathways, such as those associated with lipid and amino acid metabolism.

[This corrects the article DOI: 10.1016/j.lanwpc.2023.100846.].

OBJECTIVE:Although 5-Hydroxytryptamine (5-HT) indirectly stimulates muscle contraction and participates in regulating Acetylcholine receptor (AChR) cluster homeostasis in cellular, animal, and clinical studies, evidence regarding its potential to modulate muscle contraction in myasthenia gravis (MG) remains limited. We aim to determine the levels of 5-HT in MG and investigate its potential role as a regulatory neurotransmitter in promoting muscle contraction. METHODS:We collected serum from 109 patients with MG and 110 healthy volunteers, and recorded clinical variables, including myasthenia gravis classification (MGFA), quantitative myasthenia gravis score (QMG), and serological examination. The effects of 5-HT on the neuromuscular junction (NMJ) were further identified using cellular and molecular experiments. RESULTS:In this study, we observed that serum 5-HT levels decrease in patients with MG (p < 0.0001) compared with disease-free control. The thymoma-associated complications alleviated this reduction (p < 0.0001). Our functional studies showed that 5-HT promotes the development of motor (cholinergic) neuron-like axons and increases intracellular calcium peaks, which is proportional to the amount of neurotransmitter released (p < 0.0001). AChR-autoantibody treatment increases the expression of 5-HT2R mRNA in muscle tube cells (p < 0.001), and the downstream signaling pathway of 5-HT2R is involved in the regulation of AChR cluster homeostasis. INTERPRETATION:This first report of clinical characteristics and serum 5-HT levels from a cross-sectional cohort study on MG suggests that 5-HT plays a critical role in maintaining NMJ homeostasis. Additional cross-sectional data on more MG phenotypes and longitudinal monitoring data are needed to explore the role of 5-HT in the pathophysiological mechanisms of MG.

OBJECTIVES:The clinical characteristics and outcomes of myasthenia gravis (MG) with onset at age 50 years or older, which commonly referred to as late-onset MG (LOMG), in elderly patients remain incompletely understood. This study aimed to address the clinical heterogeneity within LOMG and to clarify whether very-late-onset MG (≥70 years) constitutes a distinct phenotype requiring tailored management approaches. METHODS:We analyzed data from 2783 patients enrolled in the MG Registry between April 1, 2009, and December 31, 2020. Patients with LOMG were further stratified into two subgroups: those with MG onset at age 50-69 years (referred to as Early-LOMG), and those with onset at age ≥70 years (referred to as advanced-onset MG, AOMG). Clinical features, diagnostic tests, treatments, and outcomes were compared across subgroups. RESULTS:Of the 982 patients with LOMG, 191 (19.4 %) were classified as AOMG. Compared to patients with MG onset at age 50-69 years, those with onset at age ≥70 years (AOMG) had a higher proportion of females (57.6 % vs 48.7 %, p = 0.027), and were more frequently positive for AChR-Ab (81.2 % vs 70.4 %, p = 0.001) and Titin-Ab (32.5 % vs 22.5 %, p = 0.004), and were more likely to present with bulbar muscle involvement at onset (25.3 % vs 14.8 %) and during disease progression (53.7 % vs 38.6 %). The positive rate of repetitive nerve stimulation (RNS) testing was also higher in the AOMG group (57.1 % vs 35.8 %, p = 0.018). Thymoma was less frequent (12.1 % vs 29.6 %, p = 0.006), and fewer AOMG patients underwent thymectomy (2.6 % vs 31.0 %, p < 0.001). AOMG patients generally required fewer immunosuppressive therapies and achieved comparable functional outcomes. However, the mortality rate was significantly higher in the AOMG group (p = 0.020), primarily due to MG crisis. CONCLUSIONS:AOMG exhibits distinct clinical features compared to Early-LOMG, characterized by a higher frequency of bulbar involvement, lower thymoma prevalence, less aggressive treatment, and higher mortality. Tailored management strategies are warranted for elderly patients with MG.

This study identified novel autoantibodies in patients with seronegative myasthenia gravis (SNMG).Autoantibodies in SNMG sera were screened using a targeted binding assay (TBA). The target antigen was identified via immunoprecipitation and mass spectrometry, and validated by western blotting using a commercial antigen. A cell-based assay (CBA) employing HEK293 cells expressing the identified antigen was established to detect specific antibodies in 676 MG patients and 20 controls.Aldolase A (ALDOA) was identified as a novel autoantigen. Anti-ALDOA antibodies (ALDOA-Ab) demonstrated high diagnostic specificity in SNMG and were also detected in seropositive MG patients, with positivity rates of 4.89% in AChR-Ab’ and 2.86% in MuSK-Ab’ subgroups. ALDOA-Ab was predominantly of the IgG1 subclass. ALDOA-Ab may serve as a potential diagnostic biomarker for MG. Further studies are needed to investigate its pathogenic role.

The gut microbiota has been closely associated with the pathogenesis of colorectal cancer (CRC). However, precise identification of particular microorganisms promoting CRC carcinogenesis, and more importantly those blocking tumor development, has been challenging based on human gut microbiota profiling studies. With a well-established azoxymethane/dextran sodium sulfate induction murine CRC model, we found a subset of mice consistently failed to develop CRC. This genetically homogeneous but cancer-refractory population gave us a unique opportunity to reveal that the microbial compositions between mice with and without CRC formation are indeed distinct, indicating key different gut microbiota between those groups are responsible for the differential susceptibility of the animals to CRC development. Our analysis revealed that Ruminococcus flavefaciens (R.f) and Fibrobacter succinogenes (F.s) were significantly enriched in CRC-free mice, while the presence of Eubacterium dolichum (E.d) was dramatically reduced. The correlative evidence was further substantiated as important causal factors, with subsequent bacteria intragastric administration experiments demonstrating independent, protective roles of R.f and F.s and a correspondingly detrimental role of E.d in inflammation-induced CRC initiation. Notably, E.d strongly activates NF-κB and promotes the local accumulation of myeloid-derived suppressor cells and macrophages. Significant disturbance of gut immune homeostasis, therefore, might be a critical trigger leading to subsequent CRC development. These findings indicate a clear direction for precise and rational gut microbiota-mediated CRC prevention.IMPORTANCEThere is a complex ecosystem of different microbes residing within the gut, which is highly relevant to health and diseases. The causal linkage between specific gut microbes and the development of colorectal cancer has been established with a mouse model, pinpointing specific bacteria species either promoting or preventing colorectal cancer development. A key aspect of these gut residual bacteria in colorectal cancer development is through exaggerating or easing gut inflammation. Therefore, by taking probiotics composed of corresponding cancer-preventing bacteria from human microbiota, it can be an effective and economic way to reduce human colorectal cancer risks.

Despite the tremendous amount of basic knowledge in cancer immunity gained and many transitional approaches attempted, current cancer immunotherapies are still far from reaching universal effectiveness. Therefore, next-generation cancer immunotherapies would emerge from deepened mechanistic insights on the full spectrum of cellular and molecular interactions between cancer cells and their immune sentinels. This review embarks on an exhaustive exploration of the cardinal immunological principles that catalyze robust cancer surveillance and their potential escapes and recapitulate the state-of-art understanding of both receptors and corresponding immune cell types involved. Both tumor intrinsic and tumor microenvironmental mediators of immune escapes are outlined in the context of current clinic applications. Following emphasizing the exceptional requisites that effective cancer immunity cycle must meet, specific cellular subsets crucial for igniting tumor immunity, notably effector and helper T cells alongside antigen presentation cells are examined, focusing on their close interactions in both antigen-dependent and -independent manners. Such intricate interactions form dynamic immune hubs at the tumor site, holding promising key functionality in rendering effective cancer retreat. Grounded on these recent insights, refined immunotherapeutic strategies, especially those bolstering priming based anticancer effector functions are advocated.

This study aimed to investigate serum neurofilament light chain (sNFL) levels in patients with myasthenia gravis (MG) and explore its potential as a biomarker for disease stratification. A total of 60 MG patients and 29 normal controls (NCs) were enrolled, with no significant differences in age or gender between the two groups. MG patients were stratified by MGFA classification, QMG scores, antibody status, phenotypic subtypes, onset age, and gender. Results showed that MG patients had significantly higher sNFL levels (median: 12.7 pg./mL) compared to NCs (median: 9.1 pg./mL; p = 0.0176). Subgroup analyses revealed that sNFL levels in MGFA-II patients (median: 13.1 pg./mL) were significantly elevated compared to NCs (p = 0.0437), with no statistical difference in MGFA-I. Patients with QMG scores 7–15 (median: 13.4 pg./mL) had higher sNFL levels than those with scores 0–6 (p = 0.0207) and showed significant differences from NCs (p = 0.0023). Late-onset MG (LOMG) patients (median: 13.4 pg./mL) had higher sNFL levels than early-onset cases (p = 0.0368), and age was mildly correlated with sNFL in MG (p = 0.0477). ROC analysis showed moderate diagnostic performance of sNFL for distinguishing LOMG vs. NCs (>50 years) was 0.9464 (specificity 89.29%, sensitivity 90%), and for female MG vs. female NCs was 0.8091. In conclusion, sNFL levels are elevated in MG patients, particularly in severe and late-onset cases, suggesting its potential as a biomarker for disease stratification and severity assessment.

Myasthenia gravis (MG) is a typical autoimmune disease of the nervous system. It is characterized by skeletal muscle weakness and fatigue due to impaired neuromuscular junction transmission mediated by IgG autoantibodies. Muscle-specific receptor tyrosine kinase-associated MG (MuSK-MG), a rare and severe subtype of MG, is distinguished by the presence of anti-MuSK antibodies; it responds poorly to traditional therapies. Recent research on MuSK-MG treatment has focused on specific targeted therapies. Since B cells play a critical pathogenic role in producing autoantibodies and inflammatory mediators, they are often considered the preferred target for treating MuSK-MG. Currently, various B cell-targeted drugs have been developed to treat MuSK-MG; they have shown good therapeutic effects. This review explores the evolving landscape of B cell-targeted therapies in MuSK-MG, focusing on their mechanisms, efficacy, and safety, and the current limitations associated with their use. We discuss current B cell-targeted therapies aimed at depleting or modulating B cells via both direct and indirect approaches. Furthermore, we focus on novel and promising strategies such as Chimeric Autoantibody Receptor T cell therapy, which explicitly targets MuSK-specific B cells without compromising general humoral immunity. Finally, this review provides an outlook on the potential benefits and limitations of B cell-targeted therapy in developing new therapies for MuSK-MG. We conclude by discussing future research efforts needed to optimize these therapies, expand treatment options, and improve long-term outcomes in MuSK-MG management.

The conventional clinical therapies for autoimmune diseases (ADs) lack specificity, necessitating long-term medication that can lead to serious side effects. In contrast, chimeric antigen receptor (CAR) T cell therapy for ADs, characterized by fewer side effects and longer-lasting therapeutic effects, represents a new direction for the specific treatment of ADs. T cells modified with CAR genes possess the ability to not only secrete perforin, granzymes, and other molecules that target autoreactive immune cells but also to lead effector and regulatory T cells into autoimmune environments, thereby exerting transport, proliferation, and immune regulatory functions. Chimeric autoantibody receptor T cells can recognize and kill autoreactive cells expressing target autoantibodies through their specific antigens. In this article, we comprehensively expound on the application of CAR-T cell therapy in different ADs and summarize the current research progress in this regard. This review aims to enhance the application of CAR-T therapy in AD treatment and facilitate further studies aimed at addressing the existing gaps in CAR-T therapy for ADs.

Insufficient evidence exists to assess the effect of titin antibodies on nonthymoma myasthenia gravis (MG) treatment and prognosis. We analyzed whether titin antibody-positive patients with nonthymoma MG (non-TMG) have a higher frequency of hospitalization than those who are titin antibody-negative. We retrospectively analyzed patient data from January 2017 to July 2022 obtained from an institutional databank. We compared the clinical characteristics, treatment regimens, and MG-related annual hospitalization rate between titin antibody-positive (Titin+ group) and titin antibody-negative (Titin- group) patients with non-TMG. Multivariate logistic regression was employed to examine the factors associated with multiple hospital admissions (>= 2). Finally, 170 patients with non-TMG were included, of whom 67 (39.4%) were Titin+ and 103 (60.6%) were Titin-. Compared with the Titin- group, the Titin+ group exhibited a notably higher annual hospitalization rate (p=0.011). Multivariate logistic regression analysis revealed that titin antibody positivity was significantly associated with multiple hospitalizations. The optimal cutoff value for titin antibody levels related to multiple hospitalizations was 3.085. In patients with non-TMG, titin antibodies were associated with more frequent hospitalizations. For these patients, especially those with titers >= 3.085, close monitoring of clinical symptom changes may reduce relapse.

This study aimed to develop a new detection method for titin antibodies (titin-Ab) in patients with myasthenia gravis (MG) – a cell-based assay (CBA) that we termed titin-CBA – to improve the clinical diagnosis of MG. We detected titin-Ab in the sera of 649 patients with MG. We then compared the results with those obtained using enzyme-linked immunosorbent assay (ELISA). Among the 350 nicotinic acetylcholine receptor antibody-negative patients, ELISA detected three (0.8%) titin-Ab-positive patients, whereas titin-CBA detected four (1.1%). These results indicate that our newly established titin-Ab detection method has higher sensitivity and accuracy than ELISA when detecting titin-Ab.

In the present study, we report a novel autoantibody in patients with myasthenia gravis. TBA results showed autoantibodies targeting muscle proteins exist in the serum of the seronegative myasthenia gravis patients. ALDOA was identified as the target antigen by immunoprecipitation, mass spectrometry and Western blot. The transfected cells were used to react with the serum antibodies of MG patients. The autoantibodies may be a new biomarker for the diagnosis of MG.

Descriptions of the clinical characteristics of anti‐AChR‐MuSK‐LRP4 antibody‐negative myasthenia gravis (triple‐negative myasthenia gravis, TNMG) are lacking in the current literature. Therefore, we investigated the clinical characteristics of TNMG in Chinese patients.

PurposeThis study aimed to clarify the effect of early glucocorticoid (GC) application on achieving minimal manifestation (MM) status or better in the treatment of myasthenia gravis (MG) in the early clinical phase.MethodsA retrospective analysis was performed using data from 336 patients with MG who received GC therapy from January 2015 to September 2022 in the Zhengzhou University Henan Institute of Medical and Pharmaceutical Sciences Myasthenia Gravis Biobank (ZMB). Patients were divided into two groups: the early mono-GC group (treated with GC within 6 months of MG onset) and the delayed mono-GC group.ResultsKaplan–Meier analysis showed that the early mono-GC group achieved MM status earlier and more frequently than the delayed mono-GC group (log-rank test, p = 0.0082; hazard ratio [HR], 1.66; p = 0.011). The early mono-GC group had a lower maintenance oral GC dose than the delayed mono-GC group. In multivariate Cox regression analysis, early mono-GC (HR, 1.50; p = 0.043), early-onset MG (EOMG) (HR, 1.74; p = 0.034), and ocular MG (OMG) (HR, 1.90; p = 0.007) were associated with MM status or better. In conclusion, early mono-GC, EOMG, and OMG were positive predictors of treatment goals. In EOMG, OMG, and acetylcholine receptor antibody-positive MG (AChR-MG) subgroups, the maintenance oral GC doses in the early mono-GC group were significantly lower than the doses in the delayed mono-GC group (p < 0.05).ConclusionEarly intervention with GC led to better long-term outcomes and reduced the necessary maintenance dose of oral GC for patients with MG. EOMG and OMG were positive predictors of MM status or better with mono-GC.