Hydrogen sulfide (H₂S) is an air pollutant, having toxic effects on immune system. Necroptosis has been discussed as a new form of cell death and plays an important role in inflammation. To investigate the mechanism of H₂S-induced immune injury, and the role of microRNAs (miRNAs) in this process, based on the results of high-throughput sequencing, we selected the most significantly changed miR-15b-5p for subsequent experiments. We further predicted and determined the targeting relationship between miR-15b-5p and TGFBR3 in HD11 through miRDB, Targetscan and dual-luciferase, and found that miR-15b-5p is highly expressed in H₂S-induced necroptosis and inflammation. To understand whether miR-15b-5p/TGFBR3 axis could involve in the process of necroptosis and inflammation, we further revealed that the high expression of miR-15b-5p and the knockdown of TGFBR3 can induce necroptosis. Nec-1 treatment enhanced the survival rate of cells. Notably, H₂S exposure induces oxidative stress and activates the TGF-β pathway, which are collectively regulated by the miR-15b-5p/TGFBR3 axis. Our present study provides a new perspective for necroptosis regulated by the miR-15b-5p/TGFBR3 axis and reveals a new form of inflammation regulation in immune diseases.

硫化氢 (H ₂ S) 是一种空气污染物，对免疫系统有毒性作用。坏死性凋亡已被讨论为一种新的细胞死亡形式，并在炎症中起重要作用。为了研究H ₂ S 诱导的免疫损伤的机制，以及microRNAs（miRNAs）在这一过程中的作用，基于高通量测序结果，我们选择了变化最显着的miR-15b-5p进行后续实验。我们进一步通过miRDB、Targetscan和双荧光素酶预测并确定了miR-15b-5p与TGFBR3在HD11中的靶向关系，发现miR-15b-5p在H _{2中高表达}S 诱导的坏死性凋亡和炎症。为了了解 miR-15b-5p/TGFBR3 轴是否可能参与坏死性凋亡和炎症过程，我们进一步揭示了 miR-15b-5p 的高表达和 TGFBR3 的敲低可诱导坏死性凋亡。Nec-1 处理提高了细胞的存活率。值得注意的是，H ₂ S 暴露诱导氧化应激并激活 TGF-β 途径，这些途径共同受 miR-15b-5p/TGFBR3 轴的调节。我们目前的研究为 miR-15b-5p/TGFBR3 轴调节的坏死性凋亡提供了新的视角，并揭示了免疫疾病中炎症调节的一种新形式。