Evidence map›Paper›PMID 34012432›Full record

ArticleFrontiers in immunology2021

Increased Concentrations of Circulating Soluble MHC Class I-Related Chain A (sMICA) and sMICB and Modulation of Plasma Membrane MICA Expression: Potential Mechanisms and Correlation With Natural Killer Cell Activity in Systemic Lupus Erythematosus.

Baptiste Hervier, Matthieu Ribon, Nadine Tarantino, Julie Mussard, Magali Breckler, Vincent Vieillard, Zahir Amoura, Alexander Steinle, Reinhild Klein, Ina Kötter and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

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  6. FunctionalInternational journal of molecular sciences · 2024
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  8. Review
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  10. [Role of CD4Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2023
    Article
  11. Article
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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

11 authors at 9 institutions in 2 countries.

Baptiste HervierINSERM U1135, CNRS ERL 8255, Centre d'Immunologie et des Maladies Infectieuses (CIMI-Paris), Sorbonne Université, Paris, France.
Matthieu RibonLi2P, University Sorbonne Paris Nord, Bobigny, France.
Nadine TarantinoINSERM U1135, CNRS ERL 8255, Centre d'Immunologie et des Maladies Infectieuses (CIMI-Paris), Sorbonne Université, Paris, France.
Julie MussardLi2P, University Sorbonne Paris Nord, Bobigny, France.
Magali BrecklerLi2P, University Sorbonne Paris Nord, Bobigny, France.
Vincent VieillardINSERM U1135, CNRS ERL 8255, Centre d'Immunologie et des Maladies Infectieuses (CIMI-Paris), Sorbonne Université, Paris, France.
Zahir AmouraHôpital de la Pitié-Salpêtrière, Service de Médecine Interne 2, Centre National de Référence Maladies Systémiques Rares, Lupus et Syndrome des Anticorps Antiphospholipides, Centre National de Référence Histiocytoses, Sorbonne Université, Assistance Publique Hôpitaux de Paris, Paris, France.
Alexander SteinleInstitute for Molecular Medicine, Goethe-University Frankfurt am Main, Frankfurt am Main, Germany.
Reinhild KleinDepartment of Hematology, Oncology, Clinical Immunology and Rheumatology, University Hospital Tübingen, Tübingen, Germany.
Ina KötterDivision of Rheumatology and Systemic Inflammatory Diseases, University Hospital Hamburg-Eppendorf (UKE), Hamburg, Germany.
Patrice DeckerLi2P, University Sorbonne Paris Nord, Bobigny, France.
Inserm · FRAssistance Publique – Hôpitaux de Paris · FRCentre d'Immunologie et des Maladies Infectieuses · FRCentre National de la Recherche Scientifique · FRGoethe University Frankfurt · DEPhysiopathologie, cibles et thérapies de la polyarthrite rhumatoïdeSorbonne Université · FRUniversity Children's Hospital Tübingen · DEUniversity Medical Center Hamburg-Eppendorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is a severe autoimmune disease of unknown etiology. The major histocompatibility complex (MHC) class I-related chain A (MICA) and B (MICB) are stress-inducible cell surface molecules. MICA and MICB label malfunctioning cells for their recognition by cytotoxic lymphocytes such as natural killer (NK) cells. Alterations in this recognition have been found in SLE. MICA/MICB can be shed from the cell surface, subsequently acting either as a soluble decoy receptor (sMICA/sMICB) or in CD4

Indexed as

Lymphocyte ActivationAntibodies, AntinuclearBiomarkersCase-Control StudiesCell MembraneCells, CulturedHistocompatibility Antigens Class IHumansKiller Cells, NaturalLupus Erythematosus, SystemicNK Cell Lectin-Like Receptor Subfamily KNucleosomesPhenotypeRibonucleoproteinsSjogren's SyndromeUp-RegulationAntibodies, AntinuclearBiomarkersHistocompatibility Antigens Class IKLRK1 protein, humanMHC class I-related chain AMICB antigenNK Cell Lectin-Like Receptor Subfamily KNucleosomesRibonucleoproteinsSS-B antibodiesextracellular chromatinmonocytesnatural killer cellsplasma membrane MICAsoluble MICAsystemic lupus erythematosus

Identifiers

PMID34012432
PMCPMC8126610
OpenAlexW3157077236

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.