Kong, Yaxian
Wang, Yu
Wu, Xueying
Han, Junyan
Li, Guoli
Hua, Mingxi
Han, Kai
Zhang, Henghui
Li, Ang
Zeng, Hui
2020-09-30T19:57:16Z
2020-09-30T19:57:16Z
2020
2059-3635
https://doi.org/10.1038/s41392-020-00308-2
http://hdl.handle.net/20.500.12010/14035
As the outbreak of coronavirus disease 2019 (COVID-19) turns
into a pandemic, it has literally caused a worldwide public health
crisis. Progressive lymphopenia, especially in T cells, was a
prominent clinical feature of severe COVID-19 in addition to
dyspnea, hypoxemia, acute respiratory distress, and cytokine
release syndrome.1 Recently, several studies revealed a correlation
between T cell depletion and increased expression levels of
several inhibitory checkpoint molecules on T cells in severe
COVID-19 cases.2 Classically, inhibitory checkpoint molecules have
been documented as key factors for regulating T cell exhaustion in
a variety of chronic viral infections and tumors. Recent studies
further implied a pivotal role of inhibitory checkpoint molecules in
the pathophysiology of acute viral infections, such as Ebola virus
or hantavirus infection. Of note, soluble isoforms of checkpoints
can be produced by cleavage of membrane-bound proteins or by
alternative splicing of mRNA and competitively regulate the
functions of their membrane-bound counterparts.3 Thus it is of
great interest to determine whether soluble checkpoint molecules
are involved in immune regulation and severity of COVID-19.
3 páginas
application/pdf
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Signal Transduction and Targeted Therapy
reponame:Expeditio Repositorio Institucional UJTL
instname:Universidad de Bogotá Jorge Tadeo Lozano
COVID-19
Disease severity
Storm of soluble immune checkpoints associated with disease severity of COVID-19
Artículo
Síndrome respiratorio agudo grave
COVID-19
SARS-CoV-2
Coronavirus
info:eu-repo/semantics/openAccess
info:eu-repo/semantics/acceptedVersion
Abierto (Texto Completo)
https://doi.org/10.1038/s41392-020-00308-2
http://purl.org/coar/resource_type/c_2df8fbb1