Distinctive features of SARS-CoV-2-specific T cells predict recovery from severe COVID-19.
Distinctive features of SARS-CoV-2-specific T cells predict recovery from severe COVID-19.
复制标题
新冠病毒(SARS-CoV-2)特异性T细胞的独特特征可预测重症新冠肺炎(COVID-19)患者的康复情况。
DOI:
10.1016/j.celrep.2021.109414
复制
发表时间:
2021-07-20
期刊:
影响因子:
8.8
通讯作者:
Roan NR
中科院分区:
文献类型:
--
作者:
Neidleman J;Luo X;George AF;McGregor M;Yang J;Yun C;Murray V;Gill G;Greene WC;Vasquez J;Lee SA;Ghosn E;Lynch KL;Roan NR
Although T cells are likely players in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) immunity, little is known about the phenotypic features of SARS-CoV-2-specific T cells associated with recovery from severe coronavirus disease 2019 (COVID-19). We analyze T cells from 34 individuals with COVID-19 with severity ranging from mild (outpatient) to critical, culminating in death. Relative to individuals who succumbed, individuals who recovered from severe COVID-19 harbor elevated and increasing numbers of SARS-CoV-2-specific T cells capable of homeostatic proliferation. In contrast, fatal COVID-19 cases display elevated numbers of SARS-CoV-2-specific regulatory T cells and a time-dependent escalation in activated bystander CXCR4+ T cells, as assessed by longitudinal sampling. Together with the demonstration of increased proportions of inflammatory CXCR4+ T cells in the lungs of individuals with severe COVID-19, these results support a model where lung-homing T cells activated through bystander effects contribute to immunopathology, whereas a robust, non-suppressive SARS-CoV-2-specific T cell response limits pathogenesis and promotes recovery from severe COVID-19. Conducting CyTOF on cells from affected individuals, Neidleman et al. identify features of SARS-CoV-2-specific T cells predicting survival of severe COVID-19. Fatal COVID-19 is also characterized by escalating activation of bystander lung-homing CXCR4+ T cells. Boosting SARS-CoV-2-specific T effector responses while diminishing CXCR4-mediated homing may help recovery from severe disease.
登录
查看更多内容
影响因子:
3.1
作者:
Daniel, Volker;Naujokat, Cord;Opelz, Gerhard
通讯作者:
Opelz, Gerhard
影响因子:
32.4
作者:
Ferretti AP;Kula T;Wang Y;Nguyen DMV;Weinheimer A;Dunlap GS;Xu Q;Nabilsi N;Perullo CR;Cristofaro AW;Whitton HJ;Virbasius A;Olivier KJ Jr;Buckner LR;Alistar AT;Whitman ED;Bertino SA;Chattopadhyay S;MacBeath G
通讯作者:
MacBeath G
DOI:
10.1126/science.abd4585
发表时间:
2020-10-23
期刊:
Science (New York, N.Y.)
影响因子:
--
作者:
Bastard P;Rosen LB;Zhang Q;Michailidis E;Hoffmann HH;Zhang Y;Dorgham K;Philippot Q;Rosain J;Béziat V;Manry J;Shaw E;Haljasmägi L;Peterson P;Lorenzo L;Bizien L;Trouillet-Assant S;Dobbs K;de Jesus AA;Belot A;Kallaste A;Catherinot E;Tandjaoui-Lambiotte Y;Le Pen J;Kerner G;Bigio B;Seeleuthner Y;Yang R;Bolze A;Spaan AN;Delmonte OM;Abers MS;Aiuti A;Casari G;Lampasona V;Piemonti L;Ciceri F;Bilguvar K;Lifton RP;Vasse M;Smadja DM;Migaud M;Hadjadj J;Terrier B;Duffy D;Quintana-Murci L;van de Beek D;Roussel L;Vinh DC;Tangye SG;Haerynck F;Dalmau D;Martinez-Picado J;Brodin P;Nussenzweig MC;Boisson-Dupuis S;Rodríguez-Gallego C;Vogt G;Mogensen TH;Oler AJ;Gu J;Burbelo PD;Cohen JI;Biondi A;Bettini LR;D'Angio M;Bonfanti P;Rossignol P;Mayaux J;Rieux-Laucat F;Husebye ES;Fusco F;Ursini MV;Imberti L;Sottini A;Paghera S;Quiros-Roldan E;Rossi C;Castagnoli R;Montagna D;Licari A;Marseglia GL;Duval X;Ghosn J;HGID Lab;NIAID-USUHS Immune Response to COVID Group;COVID Clinicians;COVID-STORM Clinicians;Imagine COVID Group;French COVID Cohort Study Group;Milieu Intérieur Consortium;CoV-Contact Cohort;Amsterdam UMC Covid-19 Biobank;COVID Human Genetic Effort;Tsang JS;Goldbach-Mansky R;Kisand K;Lionakis MS;Puel A;Zhang SY;Holland SM;Gorochov G;Jouanguy E;Rice CM;Cobat A;Notarangelo LD;Abel L;Su HC;Casanova JL
通讯作者:
Casanova JL
影响因子:
168.9
作者:
Huang, Chaolin;Wang, Yeming;Cao, Bin
通讯作者:
Cao, Bin
影响因子:
6.4
作者:
Lilleri, Daniele;Fornara, Chiara;Gerna, Giuseppe
通讯作者:
Gerna, Giuseppe