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Background <p>The genetic and environmental factors influencing an individual’s susceptibility to develop Guillain–Barré syndrome (GBS) remain largely unidentified. This study aims to evaluate the genetically predicted associations between GBS and candidate autoimmune diseases using a Mendelian randomization (MR) framework.</p> Methods <p>Genetic instruments for autoimmune diseases were extracted from large-scale genome-wide association study (GWAS) datasets. Following stringent quality control, seven autoimmune diseases were ultimately retained for the primary analysis. Summary statistics for GBS were obtained from the FinnGen consortium. We employed the inverse variance weighted (IVW) method as the primary approach, supplemented by sensitivity analyses to ensure robustness. Furthermore, a high-throughput two-step MR screening of 731 immune traits was integrated to explore potential biological mediators.</p> Results <p>Genetic liability to type 1 diabetes was suggestively associated with an increased risk of GBS [OR (95% CI) = 1.26 (1.04–1.52), <i>p</i> = 0.0176]. Conversely, genetic predisposition to psoriasis vulgaris showed a suggestive protective association [OR (95% CI) = 0.784 (0.623–0.986), <i>p</i> = 0.0375]. No significant or suggestive associations were observed for rheumatoid arthritis (<i>p</i> = 0.990), sarcoidosis (<i>p</i> = 0.993), systemic lupus erythematosus (<i>p</i> = 0.240), asthma (<i>p</i> = 0.906), or Graves’ disease (<i>p</i> = 0.926). No circulating immune trait emerged as a significant mediator between these conditions.</p> Conclusion <p>This study identifies suggestive genetically predicted associations between specific autoimmune diseases and GBS susceptibility, specifically a potential risk-increasing effect of type 1 diabetes and a protective effect of psoriasis vulgaris. The absence of significant peripheral immune mediators suggests that these neuro-immune interactions may be driven by more localized or complex tissue-resident mechanisms.</p>

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Association between Guillain–Barré syndrome and 7 autoimmune diseases: a mendelian randomization study

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月9日

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  • Jialei Zhou,
  • Tong Wang,
  • Gang Chen,
  • Siyuan Yang,
  • Tianyi Wang,
  • Xiang Li Jr.

摘要

Background

The genetic and environmental factors influencing an individual’s susceptibility to develop Guillain–Barré syndrome (GBS) remain largely unidentified. This study aims to evaluate the genetically predicted associations between GBS and candidate autoimmune diseases using a Mendelian randomization (MR) framework.

Methods

Genetic instruments for autoimmune diseases were extracted from large-scale genome-wide association study (GWAS) datasets. Following stringent quality control, seven autoimmune diseases were ultimately retained for the primary analysis. Summary statistics for GBS were obtained from the FinnGen consortium. We employed the inverse variance weighted (IVW) method as the primary approach, supplemented by sensitivity analyses to ensure robustness. Furthermore, a high-throughput two-step MR screening of 731 immune traits was integrated to explore potential biological mediators.

Results

Genetic liability to type 1 diabetes was suggestively associated with an increased risk of GBS [OR (95% CI) = 1.26 (1.04–1.52), p = 0.0176]. Conversely, genetic predisposition to psoriasis vulgaris showed a suggestive protective association [OR (95% CI) = 0.784 (0.623–0.986), p = 0.0375]. No significant or suggestive associations were observed for rheumatoid arthritis (p = 0.990), sarcoidosis (p = 0.993), systemic lupus erythematosus (p = 0.240), asthma (p = 0.906), or Graves’ disease (p = 0.926). No circulating immune trait emerged as a significant mediator between these conditions.

Conclusion

This study identifies suggestive genetically predicted associations between specific autoimmune diseases and GBS susceptibility, specifically a potential risk-increasing effect of type 1 diabetes and a protective effect of psoriasis vulgaris. The absence of significant peripheral immune mediators suggests that these neuro-immune interactions may be driven by more localized or complex tissue-resident mechanisms.