病毒感染的炎症反应是抗病毒反应的重要组成部分,一个涉及CD8+T的激活和增殖的过程,CD4+T,和树突状细胞;因此,病毒感染会破坏生物体的免疫稳态,导致炎症因子释放增加。Kikuchi-Fujimoto病(KFD)是一种病因不明的炎症性自限性疾病,一般认为这种疾病的发病机制包括两个方面:病毒感染和自身免疫反应。各种免疫细胞,如CD8+T淋巴细胞,CD4+T淋巴细胞,和CD123+浆细胞样树突状细胞,以及它们诱导和分泌的细胞因子,比如干扰素,白细胞介素,和肿瘤坏死因子,在KFD的发病机制中起着至关重要的作用。在这篇文章中,我们提供了一个来自中国的年轻女性患者的案例研究,该患者表现出典型的淋巴结炎症和发烧症状。通过淋巴结活检证实了KFD的诊断。她提出了升高的ESR,IL-6和IFN-γ。病毒标志物显示巨细胞病毒(CMV)的IgG和IgM升高,EB病毒(EBV)的IgG升高,而CD4+T和CD8+T细胞计数发生变化。最终,患者通过类固醇治疗实现了疾病缓解。基于这些发现,我们对病毒感染诱导的炎症反应过程和自身免疫参与Kikuchi-Fujimoto病的发病机制进行了全面综述.
The inflammatory response to viral infection is an important component of the antiviral response, a process that involves the activation and proliferation of CD8+ T, CD4+ T, and dendritic cells; thus, viral infection disrupts the immune homeostasis of the organism, leading to an increased release of inflammatory factors. Kikuchi-Fujimoto disease (KFD) is an inflammatory self-limited disorder of unknown etiology, and it is generally believed that the pathogenesis of this disease includes two aspects: viral infection and autoimmune response. Various immune cells, such as CD8+ T lymphocytes, CD4+ T lymphocytes, and CD123+ plasmacytoid dendritic cells, as well as the cytokines they induce and secrete, such as interferons, interleukins, and tumor necrosis factors, play a crucial role in the pathogenesis of KFD. In this article, we present a
case study of a young female patient from China who exhibited typical symptoms of lymph node inflammation and fever. The diagnosis of KFD was confirmed through a lymph node biopsy. She presented with elevated ESR, IL-6, and IFN-γ. Viral markers showed elevated IgG and IgM of cytomegalovirus (CMV) and elevated IgG of Epstein-Barr virus (EBV), while changes occurred in the CD4+ T and CD8+ T cell counts. Eventually, the patient achieved disease relief through steroid treatment. Based on these findings, we conducted a comprehensive review of the involvement of viral infection-induced inflammatory response processes and autoimmunity in the pathogenesis of Kikuchi-Fujimoto disease.