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论著·临床研究 | 更新时间:2026-06-18
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PD⁃1、TIGIT在蜕膜组织CD4+ T淋巴细胞中的表达及其与不明原因复发性流产的相关性
Expressions of PD‑1 and TIGIT on decidual tissue CD4+ T lymphocytes and their correlation with unexplained recurrent miscarriage

广西医学 页码:640-648

作者机构:李抒玲,在读硕士研究生,研究方向为生殖免疫。

基金信息:国家自然科学基金(82160295);广西自然科学基金(2025GXNSFAA069695);广西医科大学第一附属医院“优秀医学英才培养计划”(202203)

DOI:10.11675/j.issn.0253⁃4304.2026.05.07

  • 中文简介
  • 英文简介
  • 参考文献

目的 分析程序性细胞死亡蛋白1(PD⁃1)及T细胞免疫球蛋白和ITIM结构域蛋白(TIGIT)在蜕膜组织CD4+ T淋巴细胞中的表达情况及其与不明原因复发性流产(URM)发生的相关性。方法 选取6例URM患者(URM组)及6例同时期非意愿妊娠要求人工流产的正常妊娠(NP)者(NP组)作为研究对象。通过实时荧光定量PCR、Western blot技术检测两组蜕膜组织中PD⁃1、TIGIT的mRNA及蛋白表达水平;通过流式细胞术检测蜕膜组织CD4+ T淋巴细胞上PD⁃1、TIGIT及其各亚群(Th1、Treg、Th2、Th17)的细胞比例,采用Spearman相关性检验分析蜕膜组织CD4+ T淋巴细胞上TIGIT及PD⁃1的表达与其各亚群细胞比例的相关性。结果 相较于NP组,URM组患者蜕膜组织中PD⁃1、TIGIT的mRNA和蛋白表达水平,以及CD4+TIGIT+ T淋巴细胞、CD4+PD⁃1+TIGIT+ T淋巴细胞和Th1细胞比例上升(P<0.05),而CD4+PD⁃1+ T淋巴细胞及Treg、Th2、Th17细胞比例差异无统计学意义(P>0.05)。CD4+TIGIT+ T淋巴细胞比例与Th1细胞比例呈正相关(P<0.05),而与Treg、Th2、Th17细胞比例无明显相关性(P>0.05);CD4+PD⁃1+ T淋巴细胞比例与Th1、Treg、Th2及Th17细胞比例无明显相关性(P>0.05)。结论 URM患者蜕膜组织中PD⁃1与TIGIT的表达上调,可能通过促进CD4+ T淋巴细胞向Th1亚群分化,从而破坏母胎界面免疫耐受,参与URM的发病过程。

Objective To analyze the expressions of programmed cell death protein 1 (PD‑1) and T cell immunoreceptor with Ig and ITIM domains (TIGIT) on decidual tissue CD4+ T lymphocytes and their correlation with the occurrence of unexplained recurrent miscarriage (URM). Methods Six patients with URM (the URM group) and six normal pregnant women (NP group) who requested artificial abortion of unintended pregnancy during the same period were enrolled. Real‑time fluorescence quantitative PCR and Western blot were adopted to detect the mRNA and protein expressions of PD‑1 and TIGIT in decidual tissue. Flow cytometry was used to detect the cell proportion of PD‑1 and TIGIT among decidual tissue CD4+ T lymphocytes and their various subsets (Th1, Treg, Th2, Th17). Spearman correlation test was used to analyze the correlations between the expressions of TIGIT and PD‑1 on decidual CD4+ T lymphocytes and the proportions of their various subsets. Results Compared with the NP group, the URM group exhibited increased mRNA and protein expressions of PD‑1 and TIGIT in decidual tissue, as well as increased proportions of CD4+TIGIT+ T lymphocytes, CD4+PD‑1+TIGIT+ T lymphocytes, and Th1 cells (P<0.05). However, there was no statistically significant difference in the proportions of CD4+PD‑1+ T lymphocytes, Treg, Th2, or Th17 cells between the two groups (P>0.05). The proportion of CD4+TIGIT+ T lymphocytes positively correlated with the proportion of Th1 cells (P<0.05), whereas it has no significant correlation with the proportions of Treg, Th2, or Th17 cells (P>0.05). The proportion of CD4+PD‑1+ T lymphocytes interpreted no significant correlation with the proportions of Th1, Treg, Th2, or Th17 cells (P>0.05). Conclusion Up-regulated expression of PD‑1 and TIGIT in decidual tissue of URM patients may disrupt maternal‑fetal immune tolerance by promoting the differentiation of CD4+ T lymphocytes toward the Th1 subset, thereby participating in the pathogenesis of URM.

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