Molecular Mimicry between SARS-CoV-2 and Human Endocrinocytes: A Prerequisite of Post-COVID-19 Endocrine Autoimmunity?
Molecular Mimicry between SARS-CoV-2 and Human Endocrinocytes: A Prerequisite of Post-COVID-19 Endocrine Autoimmunity?
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DOI：
10.3390/pathophysiology29030039
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发表时间：
2022-08-25
期刊：
影响因子：
--
通讯作者：
Utekhin VJ
中科院分区：
文献类型：
--
作者：
Churilov LP;Normatov MG;Utekhin VJ
人类和微生物/病毒/寄生虫肽之间的分子模仿是常见的，并且长期以来与外源性病原体引起的自身免疫性疾病的病因有关。近年来积累的越来越多的证据表明，SARS-CoV-2感染与自身免疫之间存在很强的相关性。本文分析了SARS-CoV-2刺突糖蛋白（s蛋白）与参与最常见自身免疫性内分泌病变的人类内分泌细胞抗原之间共享的肽的免疫原性潜力。共鉴定出SARS-CoV-2 s蛋白、甲状腺、垂体、肾上腺皮质自身抗原和朗格汉斯胰岛β细胞共有的14个五肽，均属于SARS-CoV-2的免疫反应性表位。对研究结果的讨论将结果与covid -19相关自身免疫性内分泌病变的临床相关因素联系起来。这些疾病中最常见的是自身免疫性甲状腺疾病，因此大多数共享五肽属于该疾病的标记性自身抗原。作者认为，在严重COVID-19的发病机制中，最重要的可能是针对肾上腺的自身免疫，因为肾上腺的充分反应可以防止炎症介质的过度全身作用，导致细胞因子风暴和血流动力学休克。对抗原模仿概念的批评给出了一个断言，肽共享不是保证，而只是一个先决条件，以激发基于分子模仿的自身免疫。后一事件发生在某些HLA单倍型的携带者中，当共享肽仅用于抗原处理时
Molecular mimicry between human and microbial/viral/parasite peptides is common and has long been associated with the etiology of autoimmune disorders provoked by exogenous pathogens. A growing body of evidence accumulated in recent years suggests a strong correlation between SARS-CoV-2 infection and autoimmunity. The article analyzes the immunogenic potential of the peptides shared between the SARS-CoV-2 spike glycoprotein (S-protein) and antigens of human endocrinocytes involved in most common autoimmune endocrinopathies. A total of 14 pentapeptides shared by the SARS-CoV-2 S-protein, thyroid, pituitary, adrenal cortex autoantigens and beta-cells of the islets of Langerhans were identified, all of them belong to the immunoreactive epitopes of SARS-CoV-2. The discussion of the findings relates the results to the clinical correlates of COVID-19-associated autoimmune endocrinopathies. The most common of these illnesses is an autoimmune thyroid disease, so the majority of shared pentapeptides belong to the marker autoantigens of this disease. The most important in pathogenesis of severe COVID-19, according to the authors, may be autoimmunity against adrenals because their adequate response prevents excessive systemic action of the inflammatory mediators causing cytokine storm and hemodynamic shock. A critique of the antigenic mimicry concept is given with an assertion that peptide sharing is not a guarantee but only a prerequisite for provoking autoimmunity based on the molecular mimicry. The latter event occurs in carriers of certain HLA haplotypes and when a shared peptide is only used in antigen processing
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影响因子：
7.3
作者：
Li, Ning;Aoki, Valeria;Liu, Zhi;Prisayanh, Phillip;Valenzuela, Jesus G.;Diaz, Luis A.
通讯作者：
Diaz, Luis A.
影响因子：
56.9
作者：
Matzinger, P
通讯作者：
Matzinger, P
影响因子：
1.9
作者：
Bogdanos, DP;Baum, H;Vergani, D
通讯作者：
Vergani, D
DOI：
10.1016/j.dsx.2020.11.012
发表时间：
2020-11
期刊：
Diabetes & metabolic syndrome
影响因子：
--
作者：
Boddu SK;Aurangabadkar G;Kuchay MS
通讯作者：
Kuchay MS
影响因子：
14.9
作者：
UniProt Consortium
通讯作者：
UniProt Consortium