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On-line Access: 2024-08-27

Received: 2023-10-17

Revision Accepted: 2024-05-08

Crosschecked: 2023-12-12

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 ORCID:

Denis KUZNETSOV

https://orcid.org/0000-0003-0884-848X

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Journal of Zhejiang University SCIENCE B 2023 Vol.24 No.12 P.1141-1150

http://doi.org/10.1631/jzus.B2300025


A case of vitiligo after COVID-19 vaccination: a possible role of thymic dysfunction


Author(s):  Denis KUZNETSOV, Oleg KALYUZHIN, Andrey MIRONOV, Valery NESCHISLIAEV, Anastasiia KUZNETSOVA

Affiliation(s):  GN. Gabrichevsky Scientific and Research Institute of Epidemiology and Microbiology, Moscow 125212, Russia; more

Corresponding email(s):   denis.pfa@gmail.com

Key Words:  vitiligo, COVID-19 vaccination, thymic dysfunction, autoimmunity, сomplication, stress


Denis KUZNETSOV, Oleg KALYUZHIN, Andrey MIRONOV, Valery NESCHISLIAEV, Anastasiia KUZNETSOVA. A case of vitiligo after COVID-19 vaccination: a possible role of thymic dysfunction[J]. Journal of Zhejiang University Science B, 2023, 24(12): 1141-1150.

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author="Denis KUZNETSOV, Oleg KALYUZHIN, Andrey MIRONOV, Valery NESCHISLIAEV, Anastasiia KUZNETSOVA",
journal="Journal of Zhejiang University Science B",
volume="24",
number="12",
pages="1141-1150",
year="2023",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B2300025"
}

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%A Denis KUZNETSOV
%A Oleg KALYUZHIN
%A Andrey MIRONOV
%A Valery NESCHISLIAEV
%A Anastasiia KUZNETSOVA
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A1 - Valery NESCHISLIAEV
A1 - Anastasiia KUZNETSOVA
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Abstract: 
During the coronavirus disease 2019 (COVID-19) pandemic, vaccines help control the spread of infection. To date, 47 vaccines have been approved, with another 227 candidates in various stages of development. In the short period of time since the beginning of their use, evidence has begun to emerge of complications following vaccination in the form of the development or exacerbation of a number of pathological conditions (Block et al., 2022; Haseeb et al., 2022). For example, a population-based study in France identified 1612 cases of myocarditis and 1613 cases of pericarditis requiring hospital treatment within five months of vaccination (le Vu et al., 2022).

一例由2019冠状病毒病(COVID-19)疫苗接种引发的白癜风病例及其胸腺功能障碍的作用机制分析

Denis KUZNETSOV1,Oleg KALYUZHIN2,Andrey MIRONOV1,Valery NESCHISLIAEV3,Anastasiia KUZNETSOVA3
1G.N. Gabrichevsky Scientific and Research Institute of Epidemiology and Microbiology, Moscow 125212, Russia
2I.M. Sechenov First Moscow State Medical University, Moscow 119991, Russia
3Perm State Pharmaceutical Academy, Perm 614990, Russia
摘要:最近,人们发现接种2019冠状病毒病(COVID-19)疫苗后出现了大量并发症,影响心脏、肾脏、胰腺、关节和皮肤。本文结合已报道的11例COVID-19疫苗(主要与信使RNA(mRNA)疫苗有关)接种后白癜风病例的数据和我们自己接种的1例非复制载体疫苗后的白癜风病例,分析探讨了其相关的病理机制。根据常见的原理,自身免疫性病变是通过病毒的抗原表位与某些人类蛋白质之间的分子模拟诱发的。我们认为这一过程的基础是胸腺负选择的破坏,导致自身反应性T细胞迁移到外周。在本文中,我们证实了疫苗和/或感染以及黑素细胞氧化应激是自身免疫反应的主要诱因。在这种情况下,白癜风的发病机制可被视为糖尿病或动脉粥样硬化等多种自身免疫性疾病发病机制的模型。此外,我们概述了一种病理机制,其中黑色素细胞氧化应激、自身反应性T细胞和胸腺功能障碍可作为干预策略的潜在目标。

关键词:白癜风;2019冠状病毒病疫苗;皮质醇;去氢表雄酮;自身反应性T细胞;维生素D3

Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article

Reference

[1]AktasH, ErtuğrulG, 2022. Vitiligo in a COVID-19-vaccinated patient with ulcerative colitis: coincidence? Clin Exp Dermatol, 47(1):143-144.

[2]Amiri-DashatanN, KoushkiM, ParsamaneshN, et al., 2022. Serum cortisol concentration and COVID-19 severity: a systematic review and meta-analysis. J Invest Med, 70(3):766-772.

[3]AroraJ, WangJP, WeaverV, et al., 2022. Novel insight into the role of the vitamin D receptor in the development and function of the immune system. J Steroid Biochem Mol Biol, 219:106084.

[4]AshwellJD, LuFWM, VacchioMS, 2000. Glucocorticoids in T cell development and function. Annu Rev Immunol, 18:309-345.

[5]AygunH, 2022. Vitamin D can reduce severity in COVID-19 through regulation of PD-L1. Naunyn-Schmiedeberg’s Arch Pharmacol, 395(4):487-494.

[6]Baecher-AllanC, BrownJA, FreemanGJ, et al., 2001. CD4+CD25high regulatory cells in human peripheral blood. J Immunol, 167(3):1245-1253.

[7]BarthlottT, MoncrieffeH, VeldhoenM, et al., 2005. CD25+CD4+ T cells compete with naive CD4+ T cells for IL-2 and exploit it for the induction of IL-10 production. Int Immunol, 17(3):279-288.

[8]BlockJP, BoehmerTK, ForrestCB, et al., 2022. Cardiac complications after SARS-CoV-2 infection and mRNA COVID-19 vaccination—PCORnet, United States, January 2021–January 2022. MMWR Morb Mortal Wkly Rep, 71(14):517-523.

[9]BukhariAE, 2022. New-onset of vitiligo in a child following COVID-19 vaccination. JAAD Case Rep, 22:68-69.

[10]CaroppoF, DeottoML, TartagliaJ, et al., 2022. Vitiligo worsened following the second dose of mRNA SARS-CoV-2 vaccine. Dermatol Ther, 35(6):e15434.

[11]CarterJA, StrömichL, PeaceyM, et al., 2022. Transcriptomic diversity in human medullary thymic epithelial cells. Nat Commun, 13:4296.

[12]ChenJR, LiSL, LiCY, 2021. Mechanisms of melanocyte death in vitiligo. Med Res Rev, 41(2):1138-1166.

[13]CiccareseG, DragoF, BoldrinS, et al., 2022. Sudden onset of vitiligo after COVID-19 vaccine. Dermatol Ther, 35(1):e15196.

[14]CordellW, 2020. The mechanisms linking relative hypercortisolism—the common feature across COVID-19 risks—to ARDS, septic shock, and cytokine dysregulation. SSRN, preprint.

[15]CuiTT, ZhangWG, LiSL, et al., 2019. Oxidative stress‍–induced HMGB1 release from melanocytes: a paracrine mechanism underlying the cutaneous inflammation in vitiligo. J Invest Dermatol, 139(10):2174-2184.e4.

[16]DanielsMA, TeixeiroE, GillJ, et al., 2006. Thymic selection threshold defined by compartmentalization of Ras/MAPK signalling. Nature, 444(7120):724-729.

[17]DrabkinMJ, MeyerJI, KanthN, et al., 2018. Age-stratified patterns of thymic involution on multidetector CT. J Thorac Imaging, 33(6):409-416.

[18]DuggalNA, UptonJ, PhillipsAC, et al., 2015. NK cell immunesenescence is increased by psychological but not physical stress in older adults associated with raised cortisol and reduced perforin expression. AGE, 37:11.

[19]Dumont-LagacéM, St-PierreC, PerreaultC, 2015. Sex hormones have pervasive effects on thymic epithelial cells. Sci Rep, 5:12895.

[20]FahyGM, BrookeRT, WatsonJP, et al., 2019. Reversal of epigenetic aging and immunosenescent trends in humans. Aging cell, 18(6):e13028.

[21]GordonSM, ChaixJ, RuppLJ, et al., 2012. The transcription factors T-bet and Eomes control key checkpoints of natural killer cell maturation. Immunity, 36(1):55-67.

[22]GrantWB, al AnoutiF, BoucherBJ, et al., 2022. A narrative review of the evidence for variations in serum 25-hydroxyvitamin D concentration thresholds for optimal health. Nutrients, 14(3):639.

[23]HandelAE, IraniSR, HolländerGA, 2018. The role of thymic tolerance in CNS autoimmune disease. Nat Rev Neurol, 14(12):723-734.

[24]HaseebAA, SolymanO, AbushanabMM, et al., 2022. Ocular complications following vaccination for COVID-19: a one-year retrospective. Vaccines, 10(2):342.

[25]HerzumA, MicalizziC, MolleMF, et al., 2022. New-onset vitiligo following COVID-19 disease. Skin Health Dis, 2(1):e86.

[26]HudaMN, AhmadSM, AlamJ, et al., 2019. Infant cortisol stress‍–‍response is associated with thymic function and vaccine response. Stress, 22(1):36-43.

[27]HüeS, MonteiroRC, Berrih-AkninS, et al., 2003. Potential role of NKG2D/MHC class I-related chain A interaction in intrathymic maturation of single-positive CD8 T cells. J Immunol, 171(4):1909-1917.

[28]JacqueminC, RambertJ, GuilletS, et al., 2017. Heat shock protein 70 potentiates interferon alpha production by plasmacytoid dendritic cells: relevance for cutaneous lupus and vitiligo pathogenesis. Br J Dermatol, 177(5):‍1367-1375.

[29]JacqueminC, MartinsC, LuccheseF, et al., 2020. NKG2D defines a subset of skin effector memory CD8 T cells with proinflammatory functions in vitiligo. J Invest Dermatol, 140(6):1143-1153.e5.

[30]KaminetskyJ, RudikoffD, 2021. New-onset vitiligo following mRNA-1273 (Moderna) COVID-19 vaccination. Clin Case Rep, 9(9):e04865.

[31]KimK, BangSY, IkariK, et al., 2016. Association-heterogeneity mapping identifies an Asian-specific association of the GTF2I locus with rheumatoid arthritis. Sci Rep, 6:27563.

[32]Koç YıldırımS, 2022. A new-onset vitiligo following the inactivated COVID-19 vaccine. J Cosmet Dermatol, 21(2):429-430.

[33]KrügerC, SchallreuterKU, 2012. A review of the worldwide prevalence of vitiligo in children/adolescents and adults. Int J Dermatol, 51(10):1206-1212.

[34]le VuS, BertrandM, JabagiMJ, et al., 2022. Age and sex-specific risks of myocarditis and pericarditis following Covid-19 messenger RNA vaccines. Nat Commun, 13:3633.

[35]LiuCX, YanSX, ChenHZ, et al., 2021. Association of GTF2I, NFKB1, and TYK2 regional polymorphisms with systemic sclerosis in a Chinese Han population. Front Immunol, 12:640083.

[36]López RiquelmeI, Fernández BallesterosMD, Serrano OrdoñezA, et al., 2022. COVID-19 and autoimmune phenomena: vitiligo after Astrazeneca vaccine. Dermatol Ther, 35(7):e15502.

[37]MaccaL, PeterleL, CeccarelliM, et al., 2022. Vitiligo-like lesions and COVID-19: case report and review of vaccination- and infection-associated vitiligo. Vaccines, 10(10):1647.

[38]MahdaviMRV, ArdestaniSK, RezaeiA, et al., 2021. COVID-19 patients suffer from DHEA-S sufficiency. Immunoregulation, 3(2):135-144.

[39]MantiPG, TrattaroS, CastaldiD, et al., 2022. Thymic stroma and TFII-I: towards new targeted therapies. Trends Mol Med, 28(1):67-78.

[40]NakamagoeK, FurutaJI, ShioyaA, et al., 2009. A case of vitiligo vulgaris showing a pronounced improvement after treatment for myasthenia gravis. BMJ Case Rep, 2009:bcr07.2009.2091. http://dx.doi.org/10.1136/bcr.07.2009.2091

[41]NicolaidouE, VavouliC, KoumprentziotisIA, et al., 2023. New-onset vitiligo after COVID-19 mRNA vaccination: a causal association? J Eur Acad Dermatol Venereol, 37(1):e11-e12. http://dx.doi.org/10.1111/jdv.18513

[42]NimerRM, KhabourOF, SwedanSF, et al., 2022. The impact of vitamin and mineral supplements usage prior to COVID-19 infection on disease severity and hospitalization. Bosn J Basic Med Sci, 22(5):826-832.

[43]NyceJ, 2021. Alert to US physicians: DHEA, widely used as an OTC androgen supplement, may exacerbate COVID-19. Endocr-Relat Cancer, 28(2):R47-R53.

[44]PaolinoM, KoglgruberR, CroninSJF, et al., 2021. RANK links thymic regulatory T cells to fetal loss and gestational diabetes in pregnancy. Nature, 589(7842):442-447.

[45]PostNF, LuitenRM, WolkerstorferA, et al., 2021. Does autoimmune vitiligo protect against COVID-19 disease? Exp Dermatol, 30(9):1254-1257.

[46]QiaoJJ, ZhouGG, DingYG, et al., 2011. Multiple paraneoplastic syndromes: myasthenia gravis, vitiligo, alopecia areata, and oral lichen planus associated with thymoma. J Neurol Sci, 308(1-2):177-179.

[47]RichmondJM, FrisoliML, HarrisJE, 2013. Innate immune mechanisms in vitiligo: danger from within. Curr Opin Immunol, 25(6):676-682.

[48]SchmidtAF, RubinA, MilgraumD, et al., 2022. Vitiligo following COVID-19: a case report and review of pathophysiology. JAAD Case Rep, 22:47-49.

[49]SealKH, BertenthalD, CareyE, et al., 2022. Association of vitamin D status and COVID-19-related hospitalization and mortality. J Gen Intern Med, 37(4):853-861.

[50]ShilovES, GorshkovaEA, MinnegalievaAR, et al., 2019. Splicing pattern of mRNA in thymus epithelial cells limits the transcriptome available for negative selection of autoreactive T cells. Mol Biol, 53(1):87-96.

[51]SinghR, CohenJL, AstudilloM, et al., 2022. Vitiligo of the arm after COVID-19 vaccination. JAAD Case Rep, 28:142-144.

[52]SpeeckaertR, van GeelN, 2017. Vitiligo: an update on pathophysiology and treatment options. Am J Clin Dermatol, 18(6):733-744.

[53]StrindhallJ, NilssonBO, LöfgrenS, et al., 2007. No immune risk profile among individuals who reach 100 years of age: findings from the Swedish NONA immune longitudinal study. Exp Gerontol, 42(8):753-761.

[54]ThapaP, FarberDL, 2019. The role of the thymus in the immune response. Thorac Surg Clin, 29(2):123-131.

[55]TulicMK, CavazzaE, CheliY, et al., 2019. Innate lymphocyte-induced CXCR3B-mediated melanocyte apoptosis is a potential initiator of T-cell autoreactivity in vitiligo. Nat Commun, 10:2178.

[56]UğurerE, SivazO, AltunayİK, 2022. Newly-developed vitiligo following COVID-19 mRNA vaccine. J Cosmet Dermatol, 21(4):1350-1351.

[57]WarrenS, NehalK, QuerfeldC, et al., 2015. Graft-versus-host disease-like erythroderma: a manifestation of thymoma-associated multiorgan autoimmunity. J Cutan Pathol, 42(10):663-668.

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