Prolonged activation of nasal immune cell populations and development of tissue-resident SARS-CoV-2-specific CD8+ T cell responses following COVID-19

Roukens, Anna H E; Pothast, Cilia R.; König, Marion; Huisman, Wesley; Dalebout, Tim J.; Tak, Tamar; Azimi, Shohreh; Kruize, Yvonne C. M.; Hagedoorn, Renate S.; Zlei, Mihaela; Staal, Frank J. T.; Bie, Fenna De; Dongen, Jacques J. M. van; Arbous, Sesmu M.; Zhang, Jaimie L. H.; Verheij, Maaike; Prins, Corine; Does, Anne M. van der; Hiemstra, Pieter S.; Vries, Jutte J.C. de; Janse, Jacqueline J.; Roestenberg, Meta; Myeni, Sebenzile K.; Kikkert, Marjolein; Yazdanbakhsh, Maria; Heemskerk, Mirjam H.M.; Smits, Hermelijn H.; Jochems, Simon P.

doi:10.1038/s41590-021-01095-w

Cited by 100 publications

(58 citation statements)

References 41 publications

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“…Immunogenetics of RA suggested that RA was closely associated with the regulation of T cell activation, which was ultimately determined by positive signals from costimulatory molecules and negative signals from regulatory T cells ( 47 , 48 ). The phenotype of the SARS-CoV-2-specific CD8+ T cells, revealed a strong T cell activation in COVID-19 patients, T cells exhibited a more robust activation profile in severe disease than in mild disease ( 49 , 50 ). In the cellular component experiment, MHC class II protein complex (5 genes) and MHC protein complex (5 genes) were two major GO pathways.…”

Section: Discussionmentioning

confidence: 99%

Bioinformatics and System Biology Approach to Identify the Influences of COVID-19 on Rheumatoid Arthritis

Tang

Zhang

et al. 2022

Front. Immunol.

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BackgroundSevere coronavirus disease 2019 (COVID -19) has led to a rapid increase in mortality worldwide. Rheumatoid arthritis (RA) was a high-risk factor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, whereas the molecular mechanisms underlying RA and CVOID-19 are not well understood. The objectives of this study were to analyze potential molecular mechanisms and identify potential drugs for the treatment of COVID-19 and RA using bioinformatics and a systems biology approach.MethodsTwo Differentially expressed genes (DEGs) sets extracted from GSE171110 and GSE1775544 datasets were intersected to generate common DEGs, which were used for functional enrichment, pathway analysis, and candidate drugs analysis.ResultsA total of 103 common DEGs were identified in the two datasets between RA and COVID-19. A protein-protein interaction (PPI) was constructed using various combinatorial statistical methods and bioinformatics tools. Subsequently, hub genes and essential modules were identified from the PPI network. In addition, we performed functional analysis and pathway analysis under ontological conditions and found that there was common association between RA and progression of COVID-19 infection. Finally, transcription factor-gene interactions, protein-drug interactions, and DEGs-miRNAs coregulatory networks with common DEGs were also identified in the datasets.ConclusionWe successfully identified the top 10 hub genes that could serve as novel targeted therapy for COVID-19 and screened out some potential drugs useful for COVID-19 patients with RA.

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Section: Discussionmentioning

confidence: 99%

Bioinformatics and System Biology Approach to Identify the Influences of COVID-19 on Rheumatoid Arthritis

Tang

Zhang

et al. 2022

Front. Immunol.

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“…Resident memory CD8+ T C cells specific to influenza virus are found in the nasal mucosa after a resolved infection, and these efficiently control a second infection with the influenza virus [ 20 , 67 ]. Resident memory CD8+ T C cells specific for SARS-CoV-2 persist in the nasal mucosa for at least two months after recovery from COVID-19 [ 68 ], and it seems likely that, analogous to influenza, they help resolve the infection in the URT and provide protective immunity in subsequent exposure to the virus.…”

Section: Urt Immunity After Sars-cov-2 Infectionmentioning

confidence: 99%

Innate and Adaptive Immune Responses in the Upper Respiratory Tract and the Infectivity of SARS-CoV-2

Ramasamy

2022

Viruses

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Increasing evidence shows the nasal epithelium to be the initial site of SARS-CoV-2 infection, and that early and effective immune responses in the upper respiratory tract (URT) limit and eliminate the infection in the URT, thereby preventing infection of the lower respiratory tract and the development of severe COVID-19. SARS-CoV-2 interferes with innate immunity signaling and evolves mutants that can reduce antibody-mediated immunity in the URT. Recent genetic and immunological advances in understanding innate immunity to SARS-CoV-2 in the URT, and the ability of prior infections as well as currently available injectable and potential intranasal COVID-19 vaccines to generate anamnestic adaptive immunity in the URT, are reviewed. It is suggested that the more detailed investigation of URT immune responses to all types of COVID-19 vaccines, and the development of safe and effective COVID-19 vaccines for intranasal administration, are important needs.

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“…Other groups have noted lasting changes in the T and B cell populations in the peripheral blood of adults months after COVID-19 [40][41][42] ; a recent analysis of immune cells in the nasal mucosa also revealed enrichment of activated CD38 + CD8 + TRM and CD127 + granulocytes weeks after acute infection 43 . In our analysis of both upper respiratory tissue and peripheral blood, we see prominent changes in tonsils and adenoids compared to peripheral blood, providing evidence for tissue-specific anti-viral immune responses.…”

Section: Discussionmentioning

confidence: 98%

Robust, persistent adaptive immune responses to SARS-CoV-2 in the oropharyngeal lymphoid tissue of children

Manthiram

Milanez-Almeida

et al. 2022

Preprint

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SARS-CoV-2 infection triggers adaptive immune responses from both T and B cells. However, most studies focus on peripheral blood, which may not fully reflect immune responses in lymphoid tissues at the site of infection. To evaluate both local and systemic adaptive immune responses to SARS-CoV-2, we collected peripheral blood, tonsils, and adenoids from 110 children undergoing tonsillectomy/adenoidectomy during the COVID-19 pandemic and found 24 with evidence of prior SARS-CoV-2 infection, including detectable neutralizing antibodies against multiple viral variants. We identified SARS-CoV-2-specific germinal center (GC) and memory B cells; single cell BCR sequencing showed that these virus-specific B cells were class-switched and somatically hypermutated, with overlapping clones in the adenoids and tonsils. Oropharyngeal tissues from COVID-19-convalescent children showed persistent expansion of GC and anti-viral lymphocyte populations associated with an IFN-γ-type response, with particularly prominent changes in the adenoids, as well as evidence of persistent viral RNA in both tonsil and adenoid tissues of many participants. Our results show robust, tissue-specific adaptive immune responses to SARS-CoV-2 in the upper respiratory tract of children weeks to months after acute infection, providing evidence of persistent localized immunity to this respiratory virus.

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Prolonged activation of nasal immune cell populations and development of tissue-resident SARS-CoV-2-specific CD8+ T cell responses following COVID-19

Cited by 100 publications

References 41 publications

Bioinformatics and System Biology Approach to Identify the Influences of COVID-19 on Rheumatoid Arthritis

Bioinformatics and System Biology Approach to Identify the Influences of COVID-19 on Rheumatoid Arthritis

Innate and Adaptive Immune Responses in the Upper Respiratory Tract and the Infectivity of SARS-CoV-2

Robust, persistent adaptive immune responses to SARS-CoV-2 in the oropharyngeal lymphoid tissue of children

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