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免疫细胞与吉兰-巴雷综合征之间的因果关系:一项孟德尔随机化研究

Causal relationship between immune cells and Guillain-Barré syndrome: a Mendelian randomization study.

作者信息

Liu Huaiquan, Shao Shuoshuo, Chen Bo, Yang Shili, Zhang Xinyan

机构信息

Guizhou University of Traditional Chinese Medicine, Guiyang, Guizhou, China.

出版信息

Front Neurol. 2024 Nov 12;15:1446472. doi: 10.3389/fneur.2024.1446472. eCollection 2024.

DOI:10.3389/fneur.2024.1446472
PMID:39600430
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11588641/
Abstract

OBJECTIVE

The aim of this study was to investigate the causal effect of immune cell phenotype on GBS using two-sample Mendelian randomization (MR) approach.

METHODS

This study used MR to investigate the causal relationship between 731 immune cell phenotypes and GBS. We used Inverse variance weighted, Weighted median, MR Egger, Simple mode, Weighted mode for MR analysis. We also used the Cochran Q test, MR-Egger intercept test, IVW regression and MR-PRESSO, leave-one-out analysis to assess the presence of horizontal pleiotropy, heterogeneity and stability, respectively.

RESULTS

Our study revealed a causal relationship between 33 immune cell phenotypes and GBS. Twenty immunophenotypes were observed to be associated with GBS as risk factors. For example, CD20 on IgD+ CD38dim in the B cell group (OR = 1.313, 95%CI:1.042-1.654,  = 0.021), CD3 on CD4 Treg in Treg cell group (OR = 1.395, 95%CI:1.069-1.819,  = 0.014), CD3 on TD CD8br in Maturation stages of T cell group (OR = 1.486, 95%CI:1.025-2.154,  = 0.037), CD16 on CD14+ CD16+ monocyte in Monocyte group (OR = 1.285, 95%CI:1.018-1.621,  = 0.035), CD33dim HLA DR+ CD11b + %CD33dim HLA DR+ in Myeloid cell group (OR = 1.262, 95%CI:1.020-1.561,  = 0.032), HLA DR+ NK AC in TBNK cell group (OR = 1.568, 95%CI:1.100-2.237,  = 0.013). Thirteen immune phenotypes are associated with GBS as protective factors. For example, CD19 on PB/PC in the B cell group (OR = 0.577, 95%CI:0.370-0.902,  = 0.016), CD4 Treg AC in Treg cell group (OR = 0.727, 95%CI:0.538-0.983,  = 0.038), CD11c + monocyte %monocyte in cDC group (OR = 0.704, 95%CI:0.514-0.966,  = 0.030), CX3CR1 on CD14+ CD16- monocyte in Monocyte group (OR = 0.717, 95%CI:0.548-0.939,  = 0.016), Mo MDSC AC in Myeloid cell group (OR = 0.763, 95%CI:0.619-0.939,  = 0.011), CD45 on granulocyte in TBNK group (OR = 0.621, 95%CI:0.391-0.984,  = 0.042).

CONCLUSION

The findings suggest that certain specific immune cell phenotypes, particularly B cell and Treg cell subpopulations, are causally associated with GBS, providing potential targets for the clinical treatment of GBS.

摘要

目的

本研究旨在采用两样本孟德尔随机化(MR)方法探讨免疫细胞表型对吉兰 - 巴雷综合征(GBS)的因果效应。

方法

本研究使用MR来研究731种免疫细胞表型与GBS之间的因果关系。我们使用逆方差加权法、加权中位数法、MR-Egger法、简单模式法、加权模式法进行MR分析。我们还使用 Cochr an Q检验、MR-Egger截距检验、IVW回归和MR-PRESSO、留一法分析分别评估水平多效性、异质性和稳定性的存在情况。

结果

我们的研究揭示了33种免疫细胞表型与GBS之间的因果关系。观察到20种免疫表型与GBS相关,为危险因素。例如,B细胞组中IgD + CD38dim上的CD20(OR = 1.313,95%CI:1.042 - 1.654,P = 0.021),调节性T细胞(Treg)组中CD4 Treg上的CD3(OR = 1.395,95%CI:1.069 - 1.819,P = 0.014),T细胞成熟阶段中TD CD8br上的CD3(OR = 1.486,95%CI:1.025 - 2.154,P = 0.037),单核细胞组中CD14 + CD16 +单核细胞上的CD16(OR = 1.285,95%CI:1.018 - 1.621,P = 0.035),髓样细胞组中CD33dim HLA DR + CD11b + %CD33dim HLA DR +(OR = 1.262,95%CI:1.020 - 1.561,P = 0.032),TBNK细胞组中HLA DR + NK AC(OR = 1.568,95%CI:1.100 - 2.237,P = 0.013)。13种免疫表型与GBS相关,为保护因素。例如,B细胞组中PB/PC上的CD19(OR = 0.577,95%CI:0.370 - 0.902,P = 0.016),Treg细胞组中CD4 Treg AC(OR = 0.727,95%CI:0.538 - 0.983,P = 0.038),cDC组中CD11c +单核细胞%单核细胞(OR = 0.704,95%CI:0.514 - 0.9

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d554/11588641/19afcb239bdf/fneur-15-1446472-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d554/11588641/f812fccfc6d4/fneur-15-1446472-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d554/11588641/c1d9a7e58df5/fneur-15-1446472-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d554/11588641/6aa12c2c3e26/fneur-15-1446472-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d554/11588641/1c85bca33b8c/fneur-15-1446472-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d554/11588641/b95bc81b6d83/fneur-15-1446472-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d554/11588641/915a4c0e9e67/fneur-15-1446472-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d554/11588641/19afcb239bdf/fneur-15-1446472-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d554/11588641/f812fccfc6d4/fneur-15-1446472-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d554/11588641/c1d9a7e58df5/fneur-15-1446472-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d554/11588641/6aa12c2c3e26/fneur-15-1446472-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d554/11588641/1c85bca33b8c/fneur-15-1446472-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d554/11588641/b95bc81b6d83/fneur-15-1446472-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d554/11588641/915a4c0e9e67/fneur-15-1446472-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d554/11588641/19afcb239bdf/fneur-15-1446472-g007.jpg

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