这项研究的目的是进行系统的文献综述,以研究导致植入失败的主要免疫细胞。我们选择了PubMed的论文,Embase和虚拟健康库数据库。符合条件的文章包括2010年1月1日至2022年4月24日之间的出版物。纳入标准为:观察性研究和病例对照研究;排除标准为:综述论文,给编辑的信,摘要,动物研究和病例报告。我们提取了以下信息:收集日,患者数量,对照组,患者年龄,使用的样品类型,免疫细胞和细胞因子。作为我们制图的主要发现,我们发现在外周血中,CD3+,CD4+,CD8+,CD16+,CD56+,CD57+,CD69+,CD154+,CD158a+,NKp46细胞增加,CD4+,CD45+,Foxp3和NKp46标志降低。从子宫内膜活检中,CD3+增加了,CD4+,CD5+,CD8+,CD16+,CD25+,CD45+,CD56+,CD57+,CD68+,CD127+和CD45+的减少,CD56+,NKp46和FoxP3细胞。外周血中发现的细胞因子增加包括IL-6,IL-10,IL-17,INF-γ,TGF-β,TNF-α;而IL-4,IL-6,IL-10,IL-35,FoxP3,TGF-β,SOCS3减少了。至于活检,IL-2、IL-6、IL-17、IL-22、IL-23、INF-A1、INF-B1、INF-γ、TNF-R和IL-6,IL-10,INF-γ的减少,TGFβ,TNF-α。我们得出结论,在妊娠失败期间可以调节免疫细胞,但需要进一步的研究来阐明免疫系统对这些患者子宫内膜的调节作用。
The aim of this study was to carry out a systematic literature
review to investigate the main immune cells responsible for implantation failures. We selected papers from PubMed, Embase and Virtual Health Library databases. Eligible articles included publications between January 1, 2010 and April 24, 2022. Inclusion criteria were: observational and case-control studies; and the exclusion criteria were:
review papers, letters to the editor, abstracts, animal studies and case reports. We extracted the following information: day of collection, number of patients, control group, age of patients, type of sample used, immune cells and cytokines. As main findings in our mapping, we found that in peripheral blood, CD3+, CD4+, CD8+, CD16+, CD56+, CD57+, CD69+, CD154+, CD158a+, NKp46 cells were increased and the CD4+, CD45+, Foxp3 and NKp46 markers were reduced. From the endometrial biopsies, there was an increase in CD3+, CD4+, CD5+, CD8+, CD16+, CD25+, CD45+, CD56+, CD57+, CD68+, CD127+ and a reduction in CD45+, CD56+, NKp46 and FoxP3 cells. Cytokines found increased in peripheral blood included IL-6, IL-10, IL-17, INF-γ, TGF-ß, TNF-α; while IL-4, IL-6, IL-10, IL-35, FoxP3, TGF-ß, SOCS3 were reduced. As for the biopsies, there was an increase in IL-2, IL-6, IL-17, IL-22, IL-23, INF-A1, INF-B1, INF-γ, TNF-R and a reduction in IL-6, IL-10, INF-γ, TGFß, TNF-α. We concluded that immune cells can be modulated during pregnancy failure, but further studies are needed to elucidate the modulating effect of the immune system on the endometrium of these patients.