SARS-CoV-2 vaccination induces immunological T cell memory able to cross-recognize variants from Alpha to Omicron.
SARS-CoV-2 vaccination induces immunological T cell memory able to cross-recognize variants from Alpha to Omicron.
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DOI：
10.1016/j.cell.2022.01.015
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发表时间：
2022-03-03
期刊：
影响因子：
64.5
通讯作者：
Sette A
中科院分区：
文献类型：
--
作者：
Tarke A;Coelho CH;Zhang Z;Dan JM;Yu ED;Methot N;Bloom NI;Goodwin B;Phillips E;Mallal S;Sidney J;Filaci G;Weiskopf D;da Silva Antunes R;Crotty S;Grifoni A;Sette A
我们研究了不同疫苗平台（mRNA-1273，BNT 162 b2，Ad26.COV2.S和NVX-CoV 2373）诱导的T细胞应答是否交叉识别早期SARS-CoV-2变体。对早期变体的T细胞应答在疫苗平台上得以保留。相比之下，观察到记忆B细胞和中和抗体的显著总体降低。在接种疫苗后约6个月的受试者中，通过AIM测定，平均90%（CD 4+）和87%（CD 8+）的记忆T细胞应答针对变体被保留，并且84%（CD 4+）和85%（CD 8+）针对Omicron被保留。与其他变体相比，Omicron RBD记忆B细胞识别率大幅降低至42%。T细胞表位库分析揭示了由CD 4+和CD 8 + T细胞识别的11和10个刺突表位的中值，对于Omicron平均保存> 80%。大多数T细胞反应的功能保留可能作为针对不同变体的二级防御发挥重要作用。由SARS-CoV-2疫苗诱导的人类记忆T细胞保持识别病毒变体的能力，包括Omicron变体。
We address whether T cell responses induced by different vaccine platforms (mRNA-1273, BNT162b2, Ad26.COV2.S, and NVX-CoV2373) cross-recognize early SARS-CoV-2 variants. T cell responses to early variants were preserved across vaccine platforms. By contrast, significant overall decreases were observed for memory B cells and neutralizing antibodies. In subjects ∼6 months post-vaccination, 90% (CD4+) and 87% (CD8+) of memory T cell responses were preserved against variants on average by AIM assay, and 84% (CD4+) and 85% (CD8+) preserved against Omicron. Omicron RBD memory B cell recognition was substantially reduced to 42% compared with other variants. T cell epitope repertoire analysis revealed a median of 11 and 10 spike epitopes recognized by CD4+ and CD8+ T cells, with average preservation > 80% for Omicron. Functional preservation of the majority of T cell responses may play an important role as a second-level defense against diverse variants. Human memory T cells induced by SARS-CoV-2 vaccines maintain the ability to recognize viral variants, including the Omicron variant.
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影响因子：
64.8
作者：
Mlcochova P;Kemp SA;Dhar MS;Papa G;Meng B;Ferreira IATM;Datir R;Collier DA;Albecka A;Singh S;Pandey R;Brown J;Zhou J;Goonawardane N;Mishra S;Whittaker C;Mellan T;Marwal R;Datta M;Sengupta S;Ponnusamy K;Radhakrishnan VS;Abdullahi A;Charles O;Chattopadhyay P;Devi P;Caputo D;Peacock T;Wattal C;Goel N;Satwik A;Vaishya R;Agarwal M;Indian SARS-CoV-2 Genomics Consortium (INSACOG);Genotype to Phenotype Japan (G2P-Japan) Consortium;CITIID-NIHR BioResource COVID-19 Collaboration;Mavousian A;Lee JH;Bassi J;Silacci-Fegni C;Saliba C;Pinto D;Irie T;Yoshida I;Hamilton WL;Sato K;Bhatt S;Flaxman S;James LC;Corti D;Piccoli L;Barclay WS;Rakshit P;Agrawal A;Gupta RK
通讯作者：
Gupta RK
影响因子：
3
作者：
Paul S;Arlehamn CSL;Schulten V;Westernberg L;Sidney J;Peters B;Sette A
通讯作者：
Sette A
影响因子：
64.8
作者：
Cho A;Muecksch F;Schaefer-Babajew D;Wang Z;Finkin S;Gaebler C;Ramos V;Cipolla M;Mendoza P;Agudelo M;Bednarski E;DaSilva J;Shimeliovich I;Dizon J;Daga M;Millard KG;Turroja M;Schmidt F;Zhang F;Tanfous TB;Jankovic M;Oliveria TY;Gazumyan A;Caskey M;Bieniasz PD;Hatziioannou T;Nussenzweig MC
通讯作者：
Nussenzweig MC
影响因子：
64.5
作者：
Garcia-Beltran WF;St Denis KJ;Hoelzemer A;Lam EC;Nitido AD;Sheehan ML;Berrios C;Ofoman O;Chang CC;Hauser BM;Feldman J;Roederer AL;Gregory DJ;Poznansky MC;Schmidt AG;Iafrate AJ;Naranbhai V;Balazs AB
通讯作者：
Balazs AB
影响因子：
30.3
作者：
Keeton R;Richardson SI;Moyo-Gwete T;Hermanus T;Tincho MB;Benede N;Manamela NP;Baguma R;Makhado Z;Ngomti A;Motlou T;Mennen M;Chinhoyi L;Skelem S;Maboreke H;Doolabh D;Iranzadeh A;Otter AD;Brooks T;Noursadeghi M;Moon JC;Grifoni A;Weiskopf D;Sette A;Blackburn J;Hsiao NY;Williamson C;Riou C;Goga A;Garrett N;Bekker LG;Gray G;Ntusi NAB;Moore PL;Burgers WA
通讯作者：
Burgers WA