ArticleNature communications2022
Dysfunctional Sars-CoV-2-M protein-specific cytotoxic T lymphocytes in patients recovering from severe COVID-19.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Prediction of SARS-CoV-2 exposure through T cell activation profiles.Scientific reports · 2026Article
- Systematic profiling of SARS-CoV-2 structural protein-specific T cell epitopes in Omicron infections following inactivated vaccination.iScience · 2026Article
- Tumor reactivity assessment using clonal expression reveals tumor reactive CD8Frontiers in immunology · 2026Article
- Characterization of human CMV-specific CD8Cell reports methods · 2025Article
- An mRNA vaccine against monkeypox virus inhibits infection by co-activation of humoral and cellular immune responses.Nature communications · 2025Article
- The Role of Gut Microbiota in the Modulation of Pulmonary Immune Response to Viral Infection Through the Gut-Lung Axis.Journal of inflammation research · 2025Review
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- Article
- Bulk and Single-Cell RNA Sequencing Elucidate the Etiology of Severe COVID-19.International journal of molecular sciences · 2024Review
- COVID-19 relapse associated with SARS-CoV-2 evasion from CD4iScience · 2023Article
- SARS-CoV-2 epitope-specific T cells: Immunity response feature, TCR repertoire characteristics and cross-reactivity.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
20 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although the importance of virus-specific cytotoxic T lymphocytes (CTL) in virus clearance is evident in COVID-19, the characteristics of virus-specific CTLs related to disease severity have not been fully explored. Here we show that the phenotype of virus-specific CTLs against immunoprevalent epitopes in COVID-19 convalescents might differ according to the course of the disease. We establish a cellular screening method that uses artificial antigen presenting cells, expressing HLA-A
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Registered trials
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