The immunosuppressive function of mesenchymal stem cells (MSCs) is well known. Aryl hydrocarbon receptor (AhR), a transcription factor of the bHLH/PAS family, is widely expressed in several cells and is involved in various physiological and pathological processes. Previously, we found that the expression of AhR was downregulated in MSCs isolated from mice with neutrophilic asthma and that the activation of AhR enhanced the function of MSCs to alleviate neutrophilic asthma. We hypothesized that AhR activation enhanced MSCs for their immunosuppressive function. We aimed to investigate whether AhR activation can augment the suppressive function of MSCs against splenocyte proliferation. We co-cultured MSCs or AhR-activated MSCs with splenocytes at different ratios. The results showed that AhR activation in MSCs upregulated the expression of inducible nitric oxide (iNOS), which promoted the production of nitric oxide (NO), thus enhancing the inhibitory effect on splenocyte proliferation. The NO donor S-nitroso-N-acetylpenicillamine also inhibited the proliferation of splenocytes, and the iNOS inhibitor N(G)-nitro L-arginine methyl ester and NO scavenger 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl 3-oxide partially reversed the immunosuppressive function. Our study indicates that the AhR activation of MSCs might have an important role in the regulation of splenocyte proliferation and might serve as a potential strategy for treating immune-related diseases.

中文翻译：

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2,3,7,8-四氯二苯并-对二恶英诱导的芳烃受体活化增强了间充质干细胞对脾细胞增殖的抑制作用。

间充质干细胞（MSC）的免疫抑制功能是众所周知的。芳烃受体（AhR）是bHLH / PAS家族的转录因子，在多种细胞中广泛表达，并参与各种生理和病理过程。以前，我们发现从嗜中性哮喘小鼠分离的MSC中，AhR的表达被下调，并且AhR的激活增强了MSC缓解嗜中性哮喘的功能。我们假设AhR激活增强了MSC的免疫抑制功能。我们旨在研究AhR激活是否可以增强MSC对脾细胞增殖的抑制功能。我们将脾脏细胞与脾细胞以不同比例共培养MSC或AhR激活的MSC。结果表明，MSC中的AhR激活上调了可诱导型一氧化氮（iNOS）的表达，从而促进了一氧化氮（NO）的产生，从而增强了对脾细胞增殖的抑制作用。NO供体S-亚硝基-N-乙酰青霉胺也抑制脾细胞的增殖，iNOS抑制剂N（G）-硝基L-精氨酸甲酯和NO清除剂2-苯基-4,4,5,5-四甲基咪唑啉-1 -氧化3-氧部分逆转了免疫抑制功能。我们的研究表明，MSC的AhR激活可能在脾细胞增殖的调节中起重要作用，并且可能作为治疗免疫相关疾病的潜在策略。NO供体S-亚硝基-N-乙酰青霉胺也抑制脾细胞的增殖，iNOS抑制剂N（G）-硝基L-精氨酸甲酯和NO清除剂2-苯基-4,4,5,5-四甲基咪唑啉-1 -氧化3-氧基部分逆转了免疫抑制功能。我们的研究表明，MSC的AhR激活可能在脾细胞增殖的调节中起重要作用，并且可能作为治疗免疫相关疾病的潜在策略。NO供体S-亚硝基-N-乙酰青霉胺也抑制脾细胞的增殖，iNOS抑制剂N（G）-硝基L-精氨酸甲酯和NO清除剂2-苯基-4,4,5,5-四甲基咪唑啉-1 -氧化3-氧基部分逆转了免疫抑制功能。我们的研究表明，MSC的AhR激活可能在脾细胞增殖的调节中起重要作用，并且可能作为治疗免疫相关疾病的潜在策略。