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Table 2 Summary of research methods and conclusions related to MG

From: Mendelian randomization analyses of known and suspected risk factors and biomarkers for myasthenia gravis overall and by subtypes

Exposures

Methods

Conclusions

Vitamin D

Bidirectional two-sample MR

Circulating vitamin D levels had no causal effect on MG and MG had no causal effect on circulating vitamin D [36].

COVID-19

LDSC; Two-sample MR

No evidence of a genetic correlation or causal relationship among COVID-19 susceptibility, hospitalization, severity, and MG [37].

Ischemic stroke (IS)

Bidirectional two-sample MR

Bidirectional MR analysis did not provide evidence to support a causal relationship between genetically predicted MG and IS [38].

PCSK9 inhibitor

Two-sample MR

No evidence of a genetic correlation or causal relationship among PCSK9 inhibitor and MG [39].

Physical activity and sedentary behavior

LDSC; two-sample MR; MVMR

Findings support a causal effect of sedentary behavior as measured by LST on MG [40].

Five autoimmune diseases

Bidirectional two-sample MR

Results supported a bidirectional causal association between MG and SLE/T1DM [41].

Gut microbiota

Bidirectional two-sample MR

Research results yielded evidence of a causality connection in both directions between gut microbiota and myasthenia gravis [42].

T-cell traits

Two-sample MR

Three T-cell traits were identified to be causally protective for MG risk: (1) CD8 on terminally differentiated CD8+ T cells; (2) CD4+ regulatory T proportion in T cells; (3) HVEM expression on total T cells and other eight T-cell subtypes (e.g., naïve CD4+ T cells) [16].

  1. LDSC: linkage disequilibrium score; MVMR: multivariable extension analyses; LST: leisure screen time; SLE: systemic lupus erythematosus; T1DM: type 1 diabetes