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基碳化合物受体差异调节人类B细胞系中抗体同型的表达特征

Mili S Bhakta-Yadav¹, Kaulini Burra¹, Nasser Alhamdan¹

¹Department of Pharmacology & Toxicology, Boonshoft School of Medicine, Wright State University, Dayton, Ohio 45435, USA.

Toxicological sciences : an official journal of the Society of Toxicology

|March 25, 2024

概括

阿里碳水化合物受体 (AhR) 被环境污染物 (如TCDD) 激活会抑制人类IgG抗体的分泌. 然而,AhR对抗性会增强IgG和IgA的产生,这表明AhR调节会影响免疫功能.

科学领域:

免疫学免疫学免疫学
环境健康环境健康
毒理学毒理学毒理学

背景情况:

2,3,7,8-四二二氧化 (TCDD) 是一种持续性环境污染物.
在动物模型中,TCDD与酸受体 (AhR) 结合,其激活通常会抑制动物模型中的抗体分泌.
对于AhR激活对人类抗体产生的影响尚不清楚.

研究的目的:

研究AhR激活和对抗作用对人类免疫球蛋白 (Ig) 同型表达和分泌的影响.
为了确定CD40L+IL-4刺激在AhR调节器的存在下如何影响这些过程.

主要方法:

利用一种能够产生Ig分泌和类交换机再组合的人类伯基特淋巴瘤B细胞系 (CL-01).
暴露于AhR激动剂 (TCDD,因德鲁) 和抗剂 (CH223191) 的细胞,有或没有CD40L+IL-4刺激.
测量Ig分泌 (IgM,IgA,IgG) 和Ig重链 (IgH) 常数区域基因表达 (Cμ,Cγ,Cα,Cε).

主要成果:

艾哈激动剂对IgM和IgA分泌的影响很小,但显著抑制了刺激诱导的IgG分泌.
激活AhR可以抑制IgG (Cγ2-4) 和IgE (Cε) 的mRNA转录,但不能抑制IgM (Cμ) 或IgA (Cα2).
AhR对抗逆转了TCDD诱导的抑制,特别是增加了IgG和IgA分泌和Cγ/Cε表达,而不依赖于刺激.

结论:

由于细胞刺激的影响,AhR调节对人类IgH同型表达和抗体分泌有差异性影响.
改变AhR活性的环境暴露可能直接影响人类免疫功能和与抗体相关的疾病.
AhR对抗是一种增强抗体产生,特别是IgG和IgA的潜在策略.

关键词:

乙型淋巴细胞B型淋巴细胞在TCDD/二氧化中.产生抗体的生产.阿里碳水化合物受体是什么?免疫球体蛋白重链免疫球体蛋白重链免疫球体蛋白交易活化交易活化

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