This study investigated the role of interleukin (IL)‐9 and IL‐10 in the pathogenesis of chronic spontaneous urticaria (CSU). Autologous serum skin test and histamine release test were performed in CSU patients and normal subjects. Kunming mice were used to develop a mouse model for CSU. We induced IL‐9 overexpression, IL‐10 overexpression, and JAK/STAT pathway inhibition as well as a combination of all three conditions in CSU and control mice. Eosinophils in the skin tissues, inflammatory cytokine expression, and distribution of T lymphocyte subsets in peripheral blood of mice were detected. Expression patterns of IL‐9, IL‐10, STAT3, JAK2, and INF‐γ in clinical samples and mice were detected by reverse transcription quantitative polymerase chain reaction (RT‐qPCR) and western blot analysis. The positive rate of autologous serum skin test and the histamine release rate of CSU patients, compared with normal subjects, were apparently elevated. Compared with controls, mice with CSU experienced longer duration and higher frequency of pruritus and demonstrated enhanced levels of CD8⁺, the ratio of CD4⁺/CD8⁺, number of eosinophils, and inflammatory cytokine expression in serum as well as activated JAK/STAT signalling pathway; at the same time, levels of CD4⁺ and INF‐γ were reduced. This trend was found in CSU mice overexpressing IL‐9 and IL‐10 when compared with the CSU mice without treatment. In contrast, JAK/STAT inhibition reversed the above trend. Overall, our study suggests that IL‐9 and IL‐10 contribute to CSU development via activation of the JAK/STAT signalling pathway.

中文翻译：

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IL-9和IL-10通过JAK / STAT信号通路在慢性自发性荨麻疹发病机制中的作用。

这项研究调查了白介素（IL）-9和IL-10在慢性自发性荨麻疹（CSU）发病机理中的作用。在CSU患者和正常受试者中进行自体血清皮肤测试和组胺释放测试。昆明小鼠用于建立CSU的小鼠模型。我们在CSU和对照小鼠中诱导了IL-9的过表达，IL-10的过表达和JAK / STAT通路抑制以及所有这三种情况的组合。检测小鼠皮肤组织中的嗜酸性粒细胞，炎性细胞因子表达以及小鼠外周血中T淋巴细胞亚群的分布。通过逆转录定量聚合酶链反应（RT-qPCR）和Western印迹分析检测了临床样品和小鼠中IL-9，IL-10，STAT3，JAK2和INF-γ的表达模式。与正常人相比，CSU患者的自体血清皮肤试验阳性率和组胺释放率明显升高。与对照组相比，患有CSU的小鼠经历了更长的持续时间和更高的瘙痒发生率，并表现出CD8水平升高⁺，CD4 ⁺ / CD8 ⁺的比例，嗜酸性粒细胞数量和血清中炎性细胞因子的表达以及活化的JAK / STAT信号通路；同时，CD4 ⁺和INF-γ的水平降低了。与未经治疗的CSU小鼠相比，这种趋势在过表达IL-9和IL-10的CSU小鼠中发现。相反，JAK / STAT抑制逆转了上述趋势。总体而言，我们的研究表明IL-9和IL-10通过激活JAK / STAT信号传导途径促进CSU的发展。