PDF(Pubmed)
Abstract：
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.
CONCLUSIONS: COVID-19 infection is a potential trigger for relapsing polychondritis, an autoimmune disease affecting cartilage, and must be considered as a rare post-COVID complication.The hyperactive immune system in autism spectrum disorder (ASD) is an important predisposing factor to the induction of more autoimmune diseases after the occurrence of post-infectious dysregulation.Lymphocytopenia-induced proliferation possibly initiates the post-infection immune dysregulation.
CONCLUSIONS: COVID-19 infection is a potential trigger for relapsing polychondritis, an autoimmune disease affecting cartilage, and must be considered as a rare post-COVID complication.The hyperactive immune system in autism spectrum disorder (ASD) is an important predisposing factor to the induction of more autoimmune diseases after the occurrence of post-infectious dysregulation.Lymphocytopenia-induced proliferation possibly initiates the post-infection immune dysregulation.
摘要：
COVID-19大流行后，感染后自身免疫性疾病的发病率一直在上升。最近,一名自闭症患者入院，出现轻度上呼吸道感染COVID-19。恢复和聚合酶链反应阴性后的几个月，患者出现HEp-2细胞阳性，并出现复发性多软骨炎（RP），一种罕见的自身免疫性疾病.这种自身免疫入侵的机制最终是由激活无数的免疫反应引起的。淋巴细胞减少症几乎总是伴随着各种临床形式的COVID-19；然而，它可能通过激活白细胞介素-6(IL-6)驱动淋巴细胞减少症诱导的自身反应性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反应促进自身免疫性疾病，和中性粒细胞胞外陷阱通过细胞-细胞相互作用调节免疫反应。此外，自闭症谱系障碍患者表现出免疫系统改变,包括炎性细胞因子环境增强,导致促炎Th1/Th2比例增加.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，这些患者的易感过度的免疫系统也必须被认为是感染后自身免疫性疾病发展的易感因素。
结论：COVID-19感染是复发性多软骨炎的潜在诱因，一种影响软骨的自身免疫性疾病，必须考虑为一种罕见的COVID后并发症。自闭症谱系障碍（ASD）中的过度活跃免疫系统是感染后失调发生后诱发更多自身免疫性疾病的重要诱发因素。淋巴细胞减少诱导的增殖可能引发感染后免疫失调。
结论：COVID-19感染是复发性多软骨炎的潜在诱因，一种影响软骨的自身免疫性疾病，必须考虑为一种罕见的COVID后并发症。自闭症谱系障碍（ASD）中的过度活跃免疫系统是感染后失调发生后诱发更多自身免疫性疾病的重要诱发因素。淋巴细胞减少诱导的增殖可能引发感染后免疫失调。
