Marked T cell activation, senescence, exhaustion and skewing towards TH17 in patients with COVID-19 pneumonia

dc.creatorDe Biasi, Sara
dc.creatorMeschiari, Marianna
dc.creatorGibellini, Lara
dc.creatorBellinazzi, Caterina
dc.creatorBorella, Rebecca
dc.creatorFidanza, Lucia
dc.creatorGozzi, Licia
dc.creatorIannone, Anna
dc.creatorLo Tartaro, Domenico
dc.creatorMattioli, Marco
dc.creatorPaolini, Annamaria
dc.creatorMenozzi, Marianna
dc.creatorMilić, Jovana
dc.creatorFranceschi, Giacomo
dc.creatorFantini, Riccardo
dc.creatorTonelli, Roberto
dc.creatorSita, Marco
dc.creatorSarti, Mario
dc.creatorTrenti, Tommaso
dc.creatorBrugioni, Lucio
dc.creatorCicchetti, Luca
dc.creatorFacchinetti, Fabio
dc.creatorPietrangelo, Antonello
dc.creatorClini, Enrico
dc.creatorGirardis, Massimo
dc.creatorGuaraldi, Giovanni
dc.creatorMussini, Cristina
dc.creatorCossarizza, Andrea
dc.date.accessioned2020-07-22T20:42:14Z
dc.date.available2020-07-22T20:42:14Z
dc.date.created2020-07-06
dc.description.abstractenglishThe immune system of patients infected by SARS-CoV-2 is severely impaired. Detailed investigation of T cells and cytokine production in patients affected by COVID-19 pneumonia are urgently required. Here we show that, compared with healthy controls, COVID-19 patients’ T cell compartment displays several alterations involving naïve, central memory, effector memory and terminally differentiated cells, as well as regulatory T cells and PD1+CD57+ exhausted T cells. Significant alterations exist also in several lineage-specifying transcription factors and chemokine receptors. Terminally differentiated T cells from patients proliferate less than those from healthy controls, whereas their mitochondria functionality is similar in CD4+ T cells from both groups. Patients display significant increases of proinflammatory or anti-inflammatory cytokines, including T helper type-1 and type-2 cytokines, chemokines and galectins; their lymphocytes produce more tumor necrosis factor (TNF), interferon-γ, interleukin (IL)-2 and IL-17, with the last observation implying that blocking IL-17 could provide a novel therapeutic strategy for COVID-19.spa
dc.format.extent17 páginasspa
dc.format.mimetypeapplication/pdfspa
dc.identifier.doihttps://doi.org/10.1038/s41467-020-17292-4spa
dc.identifier.issn2041-1723spa
dc.identifier.otherhttps://www.nature.com/articles/s41467-020-17292-4spa
dc.identifier.urihttps://hdl.handle.net/20.500.12010/10984
dc.publisherScience Directeng
dc.rights.accessrightsinfo:eu-repo/semantics/openAccessspa
dc.sourcereponame:Expeditio Repositorio Institucional UJTLspa
dc.sourceinstname:Universidad de Bogotá Jorge Tadeo Lozanospa
dc.subjectNeumoníaspa
dc.subject.keywordPneumoniaspa
dc.subject.lembSíndrome respiratorio agudo gravespa
dc.subject.lembCOVID-19spa
dc.subject.lembSARS-CoV-2spa
dc.subject.lembCoronavirusspa
dc.titleMarked T cell activation, senescence, exhaustion and skewing towards TH17 in patients with COVID-19 pneumoniaspa
dc.type.hasversioninfo:eu-repo/semantics/acceptedVersionspa
dc.type.localArtículospa

Archivos

Bloque original

Mostrando 1 - 1 de 1
Cargando...
Miniatura
Nombre:
s41467-020-17292-4.pdf
Tamaño:
5.88 MB
Formato:
Adobe Portable Document Format
Descripción:
Ver documento

Bloque de licencias

Mostrando 1 - 1 de 1
Cargando...
Miniatura
Nombre:
license.txt
Tamaño:
2.87 KB
Formato:
Item-specific license agreed upon to submission
Descripción: