Characterization of T lymphocytes in severe COVID‐19 patients

Fenoglio, Daniela; Dentone, Chiara; Parodi, Alessia; Biagio, Antonio Di; Bozzano, Federica; Vena, Antonio; Fabbi, Marina; Ferrera, Francesca; Altosole, Tiziana; Bruzzone, Bianca; Giacomini, Mauro; Pelosi, Paolo; Maria, Andrea De; Bassetti, Matteo; Palma, Raffaele De; Filaci, Gilberto

doi:10.1002/jmv.27037

Cited by 26 publications

(26 citation statements)

References 20 publications

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“…The frequencies of PD-1 + ICOS + cTfh, cytotoxic CD4 + T and exhausted T cells were strongly expanded in COVID-19 patients, particularly in severe patients compared to healthy individuals, which suggested that extensive T cell dysfunction was associated with COVID-19 severity (162). In severe COVID-19 patients, the frequencies of CCR6 + cTfh cells and CCR4 + cTfh cells were expanded, but CCR3 + cTfh cells and Th1 cells were low in severe COVID-19 patients compared to healthy individuals (163). The frequencies of PD-1 + ICOS + cTfh cells, activated cTfh cells and cytotoxic CD8 + T cells were strongly upregulated in COVID-19 patients, particularly in severe patients compared to healthy donors.…”

Section: Tfh Cells In Sars-cov-2 Infection and Vaccinementioning

confidence: 94%

Follicular Helper T Cells in the Immunopathogenesis of SARS-CoV-2 Infection

et al. 2021

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Coronavirus disease 2019 (COVID-19), caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is a serious infectious disease that has led to a global pandemic with high morbidity and mortality. High-affinity neutralizing antibody is important for controlling infection, which is closely regulated by follicular helper T (Tfh) cells. Tfh cells play a central role in promoting germinal center reactions and driving cognate B cell differentiation for antibody secretion. Available studies indicate a close relationship between virus-specific Tfh cell-mediated immunity and SARS-CoV-2 infection progression. Although several lines of evidence have suggested that Tfh cells contribute to the control of SARS-CoV-2 infection by eliciting neutralizing antibody productions, further studies are needed to elucidate Tfh-mediated effector mechanisms in anti-SARS-CoV-2 immunity. Here, we summarize the functional features and roles of virus-specific Tfh cells in the immunopathogenesis of SARS-CoV-2 infection and in COVID-19 vaccines, and highlight the potential of targeting Tfh cells as therapeutic strategy against SARS-CoV-2 infection.

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Section: Tfh Cells In Sars-cov-2 Infection and Vaccinementioning

confidence: 94%

Follicular Helper T Cells in the Immunopathogenesis of SARS-CoV-2 Infection

et al. 2021

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“…The low levels of somatic hypermutation among responding B cells following severe infection is consistent with an impaired GC response and may lead to the production of antibodies that are unable to mediate disease resolution. However, a robust circulating T FH cell response is detectable in the blood of many severely infected individuals, suggesting that the GC response is not defective in all cases 54 – 56 . Impaired disease resolution in severely infected individuals may also be caused in part by impaired T cell-mediated clearance of virally infected cells 19 , 52 , 57 – 60 .…”

Section: B Cell Response To Sars-cov-2 Infectionmentioning

confidence: 99%

The germinal centre B cell response to SARS-CoV-2

2021

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The germinal centre (GC) response is critical for the generation of affinity-matured plasma cells and memory B cells capable of mediating long-term protective immunity. Understanding whether severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection or vaccination elicits a GC response has profound implications for the capacity of responding B cells to contribute to protection against infection. However, direct assessment of the GC response in humans remains a major challenge. Here we summarize emerging evidence for the importance of the GC response in the establishment of durable and broad immunity against SARS-CoV-2 and discuss new approaches to modulate the GC response to better protect against newly emerging SARS-CoV-2 variants. We also discuss new findings showing that the GC B cell response persists in the draining lymph nodes for at least 6 months in some individuals following vaccination with SARS-CoV-2 mRNA-based vaccines.

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“…On the contrary, no significant alterations were described in peripheral blood [ 115 , 116 , 48 , 49 ] for T follicular helper cells (Tfh). Data on T regulatory cells are highly heterogeneous, with some reports showing an increase while some others showing a decrease in the circulation of severe COVID-19 patients [ 117 , 118 ]. Lymphopenia occurring in severe COVID-19 affects also the B cell compartment.…”

Section: Lymphopeniamentioning

confidence: 99%

Hallmarks of immune response in COVID-19: Exploring dysregulation and exhaustion

Mazzoni

Salvati

Maggi

et al. 2021

Seminars in Immunology

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One and half year following the occurrence of COVID-19 pandemic, significant efforts from laboratories all over the world generated a huge amount of data describing the prototypical features of immunity in the course of SARS-CoV-2 infection. In this Review, we rationalize and organize the main observations, trying to define a “core” signature of immunity in COVID-19. We identified six hallmarks describing the main alterations occurring in the early infection phase and in the course of the disease, which predispose to severe illness. The six hallmarks are dysregulated type I IFN activity, hyperinflammation, lymphopenia, lymphocyte impairment, dysregulated myeloid response, and heterogeneous adaptive immunity to SARS-CoV-2. Dysregulation and exhaustion came out as the trait d’union, connecting abnormalities affecting both innate and adaptive immunity, humoral and cellular responses.

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Characterization of T lymphocytes in severe COVID‐19 patients

Cited by 26 publications

References 20 publications

Follicular Helper T Cells in the Immunopathogenesis of SARS-CoV-2 Infection

Follicular Helper T Cells in the Immunopathogenesis of SARS-CoV-2 Infection

The germinal centre B cell response to SARS-CoV-2

Hallmarks of immune response in COVID-19: Exploring dysregulation and exhaustion

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