Evidence map›Paper›PMID 34229864›Full record

ReviewHuman immunology2021

Humoral immune mechanisms involved in protective and pathological immunity during COVID-19.

Gunawan Widjaja, Abduladheem Turki Jalil, Heshu Sulaiman Rahman, Walid Kamal Abdelbasset, Dmitry O Bokov, Wanich Suksatan, Mahnaz Ghaebi, Faroogh Marofi, Jamshid Gholizadeh Navashenaq, Farhad Jadidi-Niaragh and 1 more

RetractedOpen access · greenAbstract readReview
In one paragraph

Review in Human immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
10.2field-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

17 citing papers in PubMed, 73 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 9 institutions in 8 countries.

Gunawan WidjajaUniversitas Krisnadwipayana Indonesia, Jakarta, Indonesia.
Abduladheem Turki JalilFaculty of Biology and Ecology, Yanka Kupala State University of Grodno, Grodno, Belarus.
Heshu Sulaiman RahmanCollege of Medicine, University of Sulaimani, Sulaimaniyah, Iraq; Department of Medical Laboratory Sciences, Komar University of Science and Technology, Chaq-Chaq Qularaise, Sulaimaniyah, Iraq.
Walid Kamal AbdelbassetDepartment of Health and Rehabilitation Sciences, College of Applied Medical Sciences, Prince Sattam bin Abdulaziz University, Al Kharj, Saudi Arabia; Department of Physical Therapy, Kasr Al-Aini Hospital, Cairo University, Giza, Egypt.
Dmitry O BokovSechenov First Moscow State Medical University, 8 Trubetskaya St., bldg. 2, Moscow 119991, Russian Federation.
Wanich SuksatanFaculty of Nursing, HRH Princess Chulabhorn College of Medical Science, Chulabhorn Royal Academy, Bangkok 10210, Thailand.
Mahnaz GhaebiDepartment of Immunology, School of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran.
Faroogh MarofiDepartment of Hematology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Jamshid Gholizadeh NavashenaqNoncommunicable Diseases Research Center, Bam University of Medical Sciences, Bam, Iran.
Farhad Jadidi-NiaraghImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Majid AhmadiStem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Electronic address: ahmadi.m@tbzmed.ac.ir.
Tabriz University of Medical Sciences · IRAmerican University of Iraq Sulaimani · IQBam University of Medical Sciences · IRChulabhorn Hospital · THPrince Sattam Bin Abdulaziz University · SASechenov University · RUUniversitas Krisnadwipayana · IDYanka Kupala State University of Grodno · BYZanjan University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causing COVID-19 is associated with excessive inflammation, as a main reason for severe condition and death. Increased inflammatory cytokines and humoral response to SARS-CoV-2 correlate with COVID-19 immunity and pathogenesis. Importantly, the levels of pro-inflammatory cytokines that increase profoundly in systemic circulation appear as part of the clinical pictures of two overlapping conditions, sepsis and the hemophagocytic syndromes. Both conditions can develop lethal inflammatory responses that lead to tissue damage, however, in many patients hemophagocytic lymphohistiocytosis (HLH) can be differentiated from sepsis. This is a key issue because the life-saving aggressive immunosuppressive treatment, required in the HLH therapy, is absent in sepsis guidelines. This paper aims to describe the pathophysiology and clinical relevance of these distinct entities in the course of COVID-19 that resemble sepsis and further highlights two effector arms of the humoral immune response (inflammatory cytokine and immunoglobulin production) during COVID-19 infection.

Indexed as

AnimalsCOVID-19CytokinesHumansImmunity, HumoralInflammationLymphohistiocytosis, HemophagocyticSARS-CoV-2SepsisCytokines2019 novel coronavirus disease (COVID-19)Antibody responseHemophagocytic lymphohistiocytosis (HLH)SepsisSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2)

Identifiers

PMID34229864
PMCPMC8245343
OpenAlexW3180253783

What OpenQuestion holds

Textmetadata
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.