■免疫系统在甲状腺癌(THCA)的发展和治疗中起着重要作用。然而,免疫细胞与THCA的相关性尚未得到系统研究。
■这项研究使用了两个样本的孟德尔随机化(MR)研究,以确定免疫细胞特征与THCA之间的因果关系。基于大量公开的遗传数据样本,我们探讨了731种免疫细胞特征与THCA风险之间的因果关系.将731种免疫表型分为7组,包括B细胞面板(n=190),cDC面板(n=64),T细胞组的成熟期(n=79),单核细胞面板(n=43),髓系细胞组(n=64),TBNK面板(n=124),和Treg面板(n=167)。对结果的敏感性进行了分析,并排除异质性和水平多效性。
■FDR校正后,免疫表型对THCA的影响无统计学意义。值得一提的是,然而,有一些未经调整的低P值表型。单核细胞CD62L对THCA风险的比值比(OR)为0.953(95%CI=0.930~0.976,P=1.005×10-4),ThCA风险的Treg%CD4的静息估计为0.975(95%CI=0.961-0.989,P=7.984×10-4)。此外,THCA与以下5种免疫表型的风险降低相关:CD39上的CD25+Treg上的CD4(OR=0.871,95%CI=0.812~0.935,P=1.274×10-4),活化的TregAC(OR=0.884,95%CI=0.820~0.953,P=0.001),激活和静息Treg%CD4Treg(OR=0.872,95CI=0.811〜0.937,P=2.109×10-4),CD28-CD25+CD8brAC(OR=0.867,95%CI=0.809~0.930,P=6.09×10-5),CD28-CD127-CD25++CD8brAC(OR=0.875,95CI=0.814~0.942,P=3.619×10-4)。THCA与IgD+CD24+分泌Treg%CD4Treg(OR=1.143,95%CI=1.064~1.229,P=2.779×10-4)和CD19的风险增加相关(OR=1.118,95%CI=1.041~1.120,P=0.002)。
■这些发现表明了免疫细胞与THCA之间通过遗传手段的因果关系。我们的研究结果可能为未来的临床研究提供指导。
UNASSIGNED: The immune system plays an important role in the development and treatment of thyroid cancer(THCA).However, the correlation between immune cells and THCA has not been systematically studied.
UNASSIGNED: This study used a two-sample Mendelian randomization (MR) study to determine the causal relationship between immune cell characteristics and THCA. Based on a large sample of publicly available genetic data, we explored the causal relationship between 731 immune cell characteristics and THCA risk. The 731 immunophenotypes were divided into 7 groups, including B cell panel(n=190),cDC panel(n=64),Maturation stages of T cell panel(n=79),Monocyte panel(n=43),Myeloid cell panel(n=64),TBNK panel(n=124),and Treg panel(n=167). The sensitivity of the results was analyzed, and heterogeneity and horizontal pleiotropy were excluded.
UNASSIGNED: After FDR correction, the effect of immunophenotype on THCA was not statistically significant. It is worth mentioning, however, that there are some unadjusted low P-values phenotypes. The odds ratio (OR) of CD62L on monocyte on THCA risk was estimated to be 0.953 (95% CI=0.930~0.976, P=1.005×10-4),and which was estimated to be 0.975(95% CI=0.961-0.989, P=7.984×10-4) for Resting Treg%CD4 on THCA risk. Furthermore, THCA was associated with a reduced risk of 5 immunophenotype:CD25 on CD39+ CD4 on Treg (OR=0.871, 95% CI=0.812~0.935, P=1.274×10-4), activated Treg AC (OR=0.884, 95% CI=0.820~0.953, P=0.001), activated & resting Treg % CD4 Treg (OR=0.872, 95%CI=0.811~0.937,P=2.109×10-4),CD28- CD25++ CD8br AC(OR=0.867,95% CI=0.809~0.930,P=6.09×10-5),CD28-CD127-CD25++CD8brAC(OR=0.875,95%CI=0.814~0.942,P=3.619×10-4).THCA was associated with an increased risk of Secreting Treg % CD4 Treg (OR=1.143, 95% CI=1.064~1.229, P=2.779×10-4) and CD19 on IgD+ CD24+ (OR=1.118, 95% CI=1.041~1.120, P=0.002).
UNASSIGNED: These findings suggest the causal associations between immune cells and THCA by genetic means. Our results may have the potential to provide guidance for future clinical research.