Evidence map›Paper›PMID 35584714›Full record

ArticleMicrobial pathogenesis2022

The association of decreased HLA-G

Somayeh Ramzannezhad, Mona Tarighi, Mousa Mohammadnia-Afrouzi, Soudabeh Aghapour, Mojgan Bagherzadeh, Zahra Ahmadnia, Akramossadat Hosseini, Mostafa Javanian, Housein Ghorbani, Mehdi Shahbazi

Open access · greenAbstract read
In one paragraph

Article in Microbial pathogenesis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. The immunogenetics of COVID-19.Immunogenetics · 2023
    Review
  2. Review
  3. Article
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

10 authors at 1 institution in 1 country.

Somayeh RamzannezhadImmunoregulation Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran; Department of Pathology, School of Medicine, Babol University of Medical Sciences, Babol, Iran.
Mona TarighiImmunoregulation Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran; Department of Immunology, School of Medicine, Babol University of Medical Sciences, Babol, Iran.
Mousa Mohammadnia-AfrouziImmunoregulation Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran; Department of Immunology, School of Medicine, Babol University of Medical Sciences, Babol, Iran.
Soudabeh AghapourImmunoregulation Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran; Department of Immunology, School of Medicine, Babol University of Medical Sciences, Babol, Iran.
Mojgan BagherzadehImmunoregulation Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran; Department of Immunology, School of Medicine, Babol University of Medical Sciences, Babol, Iran.
Zahra AhmadniaDepartment of Pathology, School of Medicine, Babol University of Medical Sciences, Babol, Iran.
Akramossadat HosseiniDepartment of Pathology, School of Medicine, Babol University of Medical Sciences, Babol, Iran.
Mostafa JavanianInfectious Diseases and Tropical Medicine Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran.
Housein GhorbaniImmunoregulation Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran; Department of Pathology, School of Medicine, Babol University of Medical Sciences, Babol, Iran. Electronic address: Ghorbani7958@yahoo.com.
Mehdi ShahbaziImmunoregulation Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran; Department of Immunology, School of Medicine, Babol University of Medical Sciences, Babol, Iran. Electronic address: mehdishahbazi60@yahoo.com.
Babol University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionCOVID-19 (coronavirus disease-2019) is an infectious disease caused by SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2). Immune dysregulation causes inflammation and massive production of inflammatory mediators that worsen the patients' status. Here, regulatory immune cells may ameliorate inflammation and improve the severity of the disease. MATERIALS AND

methodsA total of 76 participants were enrolled in this study and divided into 3 groups as follows: patients with moderate/severe COVID-19 (n = 25), patients with critical COVID-19 (n = 26), and healthy controls (n = 25). After blood collection, peripheral blood mononuclear cells (PBMCs) were isolated and stained by FITC-conjugated anti-CD4 monoclonal antibodies (mABs), PE-conjugated anti-HLA-G mABs, PerCPCy5.5-conjugated anti-CD14 mABs, and APC-conjugated anti-CD8 mABs.

resultsCritical COVID-19 patients had a significantly lower frequency of CD4

conclusionThe increased amount of immunomodulatory HLA-G

Indexed as

COVID-19CD8-Positive T-LymphocytesHLA-G AntigensHumansInflammationLeukocytes, MononuclearSARS-CoV-2HLA-G AntigensCOVID-19HLA-G(+) monocytesHLA-G(+) T cellsSARS-CoV-2

Identifiers

PMID35584714
PMCPMC9107627
OpenAlexW4280489977

What OpenQuestion holds

Textmetadata
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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.