中国输血杂志2025，Vol.38Issue(9)：1167-1171,5.DOI:10.13303/j.cjbt.issn.1004-549x.2025.09.007
Toll样受体3在RhD同种免疫发生中的作用研究
Study on the role of toll-like receptor 3 in RhD alloimmunization
陈思恬 1田力 2宋宁 2刘忠2
作者信息
- 1. 湖南省儿童医院 检验中心,湖南 长沙 410007||中国医学科学院输血研究所,四川 成都 610052||中国医学科学院输血不良反应研究重点实验室,四川 成都 610052
- 2. 中国医学科学院输血研究所,四川 成都 610052||中国医学科学院输血不良反应研究重点实验室,四川 成都 610052
- 折叠
摘要
Abstract
Objective To preliminarily investigate the role of toll-like receptor 3(TLR3)in RhD alloimmunization.Methods Between January 10,2018 and April 1,2019,RhD negative plasma donors were recruited for active RhD allo-immunization.A panel of four RhD 15-mer peptides was synthesized to stimulate T-cell proliferation.Peripheral blood mononuclear cells(PBMCs)were collected from successfully immunized donors(responders)and divided into an experi-mental group(pre-incubated with anti-TLR3 antibody before adding RhD peptides)and a control group(RhD peptides on-ly).PBMCs proliferation was assessed using a cell proliferation enzyme-linked immunosorbent assay(BrdU),while TLR3 and IFN-α levels in cell culture supernatants and serum were detected via ELISA.Results PBMCs proliferation was signif-icantly lower in the experimental group compared to the control group[(31 234±15 300)vs(61 225±25 073)rlu/s,P＜0.001].TLR3 expression levels in the cell culture supernatants were also reduced in the experimental group[(3.49±0.32)vs(4.01±0.35)ng/mL,P＜0.001].TLR3 protein levels were detectable in responders but undetectable in the ser-um of non-responders[(1.43±1.44)vs 0 ng/mL,P＜0.001].A strong linear correlation was observed between TLR3 and IFN-α levels in serum,described by the regression model Y=2.957X+1.004(r2=0.91,P＜0.001).Conclusion TLR3 activation may promote RhD alloimmunization by inducing IFN-α secretion,indicating a critical role of the TLR3 signaling pathway in RhD immune responses.关键词
Toll样受体3/RhD同种免疫/红细胞输血/干扰素αKey words
toll-like receptor 3/RhD alloimmunization/red blood cell transfusion/interferon-alpha分类
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陈思恬,田力,宋宁,刘忠..Toll样受体3在RhD同种免疫发生中的作用研究[J].中国输血杂志,2025,38(9):1167-1171,5.
