Evidence map›Paper›PMID 32712629›Full record

ReviewSignal transduction and targeted therapy2020

COVID-19: immunopathogenesis and Immunotherapeutics.

Li Yang, Shasha Liu, Jinyan Liu, Zhixin Zhang, Xiaochun Wan, Bo Huang, Youhai Chen, Yi Zhang

Open access · goldAbstract readReview
In one paragraph

Review in Signal transduction and targeted therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 426 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
426citing papers in PubMed, 4 pooled it
18.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

426 citing papers in PubMed, 4 syntheses or guidelines pooled it, 940 citations in OpenAlex.

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  18. Acute Empyema due toRespirology case reports · 2026
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366 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 5 institutions in 2 countries.

Li Yang *Biotherapy Center, The First Affiliated Hospital of Zhengzhou University, 450052, Zhengzhou, China.
Shasha Liu *Biotherapy Center, The First Affiliated Hospital of Zhengzhou University, 450052, Zhengzhou, China.
Jinyan LiuBiotherapy Center, The First Affiliated Hospital of Zhengzhou University, 450052, Zhengzhou, China.
Zhixin ZhangInstitute of Health Management, Health Management Center, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, 611731, Chengdu, China.
Xiaochun WanShenzhen Laboratory of Human Antibody Engineering, Institute of Biomedicine and Biotechnology, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, 518055, Shenzhen, China.
Bo HuangDepartment of Immunology & National Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences (CAMS) & Peking Union Medical College, 100005, Beijing, China.
Youhai ChenDepartment of Pathology and Laboratory Medicine, School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA.
Yi ZhangBiotherapy Center, The First Affiliated Hospital of Zhengzhou University, 450052, Zhengzhou, China. yizhang@zzu.edu.cn.ORCID http://orcid.org/0000-0001-9861-4681
First Affiliated Hospital of Zhengzhou University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNChinese Academy of Sciences · CNUniversity of Electronic Science and Technology of China · CNUniversity of Pennsylvania · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The recent novel coronavirus disease (COVID-19) outbreak, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is seeing a rapid increase in infected patients worldwide. The host immune response to SARS-CoV-2 appears to play a critical role in disease pathogenesis and clinical manifestations. SARS-CoV-2 not only activates antiviral immune responses, but can also cause uncontrolled inflammatory responses characterized by marked pro-inflammatory cytokine release in patients with severe COVID-19, leading to lymphopenia, lymphocyte dysfunction, and granulocyte and monocyte abnormalities. These SARS-CoV-2-induced immune abnormalities may lead to infections by microorganisms, septic shock, and severe multiple organ dysfunction. Therefore, mechanisms underlying immune abnormalities in patients with COVID-19 must be elucidated to guide clinical management of the disease. Moreover, rational management of the immune responses to SARS-CoV-2, which includes enhancing anti-viral immunity while inhibiting systemic inflammation, may be key to successful treatment. In this review, we discuss the immunopathology of COVID-19, its potential mechanisms, and clinical implications to aid the development of new therapeutic strategies against COVID-19.

Indexed as

BetacoronavirusCoronavirus InfectionsDisease OutbreaksImmunity, InnateImmunotherapyPandemicsPneumonia, ViralShock, SepticCOVID-19CytokinesHumansSARS-CoV-2Cytokines

Identifiers

PMID32712629
PMCPMC7381863
OpenAlexW3044898763

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.