一种罕见的 COVID-19 感染后自身免疫表现

Fatih Kaya, Tarek Alsafdi, Manar Hussam Al-Suleh
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摘要

COVID-19 大流行之后,感染后自身免疫性疾病的发病率不断上升。最近,一名自闭症患者因轻度上呼吸道系统 COVID-19 感染入院。在康复和聚合酶链反应阴性几个月后,患者出现 HEp-2 细胞阳性,并出现复发性多软骨炎(RP),这是一种罕见的自身免疫性疾病。这种自身免疫性疾病的入侵机制最终是通过激活无数的免疫反应引起的。淋巴细胞减少几乎总是伴随着各种临床形式的 COVID-19;然而,它可能会通过激活白细胞介素-6(IL-6)来驱动淋巴细胞减少引起的自反应性 T 细胞增殖。此外,感染期间高水平的中性粒细胞通过释放伴随炎症的细胞因子和趋化因子级联,以及中性粒细胞胞外捕获物通过细胞-细胞相互作用调节免疫反应,从而促进自身免疫性疾病的发生。此外,自闭症谱系障碍患者的免疫系统会发生改变,包括炎症细胞因子环境增加,导致促炎症 Th1/Th2 比率增加。此外,RP 的病理生理学主要与细胞介导的免疫反应有关;因此,这类患者易患的夸大免疫系统也必须被视为感染后自身免疫疾病的易患因素。
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A rare post-infectious autoimmune manifestation of COVID-19
The incidence of post-infectious autoimmune diseases has been on the rise following the COVID-19 pandemic. Recently, an autistic patient was admitted to the hospital presenting with a mild upper respiratory system COVID-19 infection. Months after recovery and polymerase chain reaction negativity, the patient developed HEp-2 cell positivity and presented with relapsing polychondritis (RP), a rare autoimmune disease. The mechanism of this autoimmune invasion is ultimately caused by activating a myriad of immune reactions. Lymphocytopenia almost always accompanies various clinical forms of COVID-19; however, it may drive the lymphocytopenia-induced proliferation of autoreactive T cells via the activation of interleukin-6 (IL-6). Moreover, high levels of neutrophils during infection promote autoimmune disease by releasing cytokine and chemokine cascades that accompany inflammation, and neutrophil extracellular traps regulating immune responses through cell–cell interactions. Furthermore, autism spectrum disorder patients display an altered immune system that includes an augmented inflammatory cytokine milieu leading to an increased pro-inflammatory Th1/Th2 ratio. In addition, the pathophysiology of RP is majorly associated with a cell-mediated immune reaction; thus, the predisposing exaggerated immune system of such patients must also be considered as a predisposing factor to the development of post-infectious autoimmune diseases.
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