武警医学2025，Vol.36Issue(2)：145-149,5.
孟德尔随机化方法探究免疫细胞标记物与子宫内膜异位症的关系
Relationship between immune cell markers and endometriosis explored by Mendelian Randomization method
摘要
Abstract
Objective To investigate the causal relationship between immune cell markers and endometriosis(EMs)by Men-delian randomization method.Methods Two-sample Mendelian randomization analysis(MR)was used to evaluate the causal relation-ship between 731 immune cell phenotypes and EMs.Inverse variance weighting method was used and sensitivity analysis was performed to verify the reliability of the results.Results Nine immunophenotypes were significantly associated with increased risk of EMs,inclu-ding CD127 on T cell(OR=1.063,95%CI:1.001-1.130,P=0.047),CD25 on CD28+CD4+(OR=1.149,95%CI:1.026-1.286,P=0.016),CD28 on CD39+activated Treg(OR=1.004,95%CI:1.015-1.081,P=0.004),CD33br HLA DR+CD14%CD33br HLA DR+(OR=1.035,95%CI:1.002-1.069,P=0.036),CD45 on lymphocyte(OR=1.059,95%CI:1.011-1.109,P=0.015),CD45 on NK cell(OR=1.042,95%CI:1.001-1.086,P=0.046),CM CD8br AC(OR=1.060,95%CI:1.001-1.122,P=0.046),Granulocyte AC(OR=1.060,95%CI:1.004-1.120,P=0.035)and HLA DR+NK%NK cell(OR=1.044,95%CI:1.000-1.090,P=0.049.Four immunophenotypes were significantly associated with reduced risk of EMs,,including CD8 on TD CD8br(OR=0.948,95%CI:0.903-0.996,P=0.034),DN(CD4-CD8-)%leukocyte(OR=0.959,95%CI:0.930-0.989,P=0.008),HLA DR on HLA DR+CD8br(OR=0.933,95%CI:0.882-0.988,P=0.018),HLA DR+T cell AC(OR=0.972,95%CI:0.946-0.999,P=0.039),and Naive DN(CD4-CD8-)%DN(OR=0.935,95%CI:0.878-0.995,P=0.035).The results of sensitivity analysis were consistent with the results of the main study.Conclusions There is causal relationship between immune cells and susceptibility to EMs,which provides a new direction for clinical decision making and drug development.关键词
子宫内膜异位症/免疫细胞/孟德尔随机化探究/危险作用/保护作用Key words
endometriosis/immune cell/Mendelian ran-domization inquiry/risk effect/protective effect分类
医药卫生引用本文复制引用
李佳璐,杨悦,张晓莉..孟德尔随机化方法探究免疫细胞标记物与子宫内膜异位症的关系[J].武警医学,2025,36(2):145-149,5.基金项目
首都科研发展专项项目(2020-1-5112) （2020-1-5112）
