A rare post-infectious autoimmune manifestation of COVID-19

Fatih Kaya, Tarek Alsafdi, Manar Hussam Al-Suleh
{"title":"A rare post-infectious autoimmune manifestation of COVID-19","authors":"Fatih Kaya, Tarek Alsafdi, Manar Hussam Al-Suleh","doi":"10.12890/2024_004542","DOIUrl":null,"url":null,"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.","PeriodicalId":502981,"journal":{"name":"European Journal of Case Reports in Internal Medicine","volume":"33 37","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"European Journal of Case Reports in Internal Medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.12890/2024_004542","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

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.
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
一种罕见的 COVID-19 感染后自身免疫表现
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。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
ISCHAEMIC COLITIS FROM AN UNUSUAL CAUSE: ORAL CONTRACEPTIVES THE VALUE OF ULTRASONOGRAPHY IN DETECTING GASTRIC HAEMORRHAGE EXTRAMEDULLARY PARAVERTEBRAL MASS: AN UNUSUAL PRESENTATION OF HAIRY CELL LEUKAEMIA Cutaneous Pneumocystis jirovecii infection in an allogeneic stem cell transplant recipient Brevibacillus laterosporus osteomyelitis and hardware infection in a young, immunocompetent patient successfully treated by oral minocycline and ceftriaxone via a peripherally inserted central catheter for six weeks
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1