Henoch-Schonlein purpura (HSP) is the most common systemic vasculitis of the childhood. However, its mechanisms and pathogenesis still need more exploration. Natural killer (NK) cells are innate lymphocytes, and there is a growing appreciation that cellular metabolism is important in determining the immune responsiveness of lymphocytes. Thus, we aimed to analyze the NK cells phenotype and explore the association between glucose metabolism and NK cells function in HSP patients. A total number of 64 HSP patients and 34 healthy children were included. The HSP patients were divided into two groups according to whether accompanied with nephritis or not. NK cells in HSP patients without nephritis showed a reduced frequency in peripheral blood, a down-regulated expression of activating receptors both NKp30 and NKp46, and an attenuated cytotoxic function against tumor cells. In addition, the function impairment of NK cells was shown to exacerbate in HSPN. Our data further revealed an aberrant metabolic reprogramming of NK cells in HSP patients. Upon stimulation with cytokines (IL-15, IL-12 and IL-2), NK cells from healthy controls switched to an elevated glycolysis rate to support their effector function. By contrast, the glycolysis rate of activated NK cells in HSP group was not significantly up-regulated from the resting level possibly owing to the inhibition of mTORC1. Our study found that HSP patients were accompanied with dysfunction of NK cells. We concluded that the dysfunction of NK cells in HSP patients was induced with a decreased glycolysis rate and suggested that metabolic reprogramming of NK cells might be a player in the pathogenesis of HSP.

中文翻译：

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过敏性紫癜患者糖酵解减少导致 NK 细胞功能障碍

过敏性紫癜 (HSP) 是儿童期最常见的全身性血管炎。但其机制和发病机制仍需进一步探索。自然杀伤 (NK) 细胞是先天性淋巴细胞，人们越来越认识到细胞代谢在决定淋巴细胞的免疫反应性方面很重要。因此，我们旨在分析 NK 细胞表型并探讨 HSP 患者葡萄糖代谢与 NK 细胞功能之间的关联。共包括 64 名 HSP 患者和 34 名健康儿童。根据是否伴有肾炎将HSP患者分为两组。没有肾炎的 HSP 患者的 NK 细胞在外周血中的频率降低，NKp30 和 NKp46 激活受体的表达下调，和对肿瘤细胞的减弱的细胞毒作用。此外，在 HSPN 中，NK 细胞的功能受损会加剧。我们的数据进一步揭示了 HSP 患者 NK 细胞的异常代谢重编程。在用细胞因子（IL-15、IL-12 和 IL-2）刺激后，来自健康对照的 NK 细胞转变为升高的糖酵解速率以支持其效应子功能。相比之下，HSP 组活化 NK 细胞的糖酵解率从静息水平没有显着上调，可能是由于 mTORC1 的抑制。我们的研究发现HSP患者伴有NK细胞功能障碍。我们得出结论，HSP 患者中 NK 细胞的功能障碍是由糖酵解率降低引起的，并表明 NK 细胞的代谢重编程可能是 HSP 发病机制中的一个参与者。