Evidence map›Paper›PMID 20439539›Full record

ArticleThe Journal of experimental medicine2010

Invariant NKT cells limit activation of autoreactive CD1d-positive B cells.

Fredrik Wermeling, Sara M Lind, Emilie Domange Jordö, Susanna L Cardell, Mikael C I Karlsson

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

56 citing papers in PubMed, 94 citations in OpenAlex.

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  9. Combined proinflammatory cytokine and cognate activation of invariant natural killer T cells enhances anti-DNA antibody responses.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  10. Review
  11. NKT Cells in Neurological Diseases.Frontiers in cellular neuroscience · 2019
    Review
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  14. The Janus Face of NKT Cell Function in Autoimmunity and Infectious Diseases.International journal of molecular sciences · 2018
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Fredrik WermelingDepartment of Medicine, Karolinska Institutet, 171 76 Stockholm, Sweden.
Sara M Lind
Emilie Domange Jordö
Susanna L Cardell
Mikael C I Karlsson
Karolinska Institutet · SEUniversity of Gothenburg · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Faulty activation of autoreactive B cells is a hallmark of autoimmune diseases like systemic lupus erythematosus (SLE). An important feature restricting activation of autoreactive B cells is efficient removal of apoptotic material. Mounting evidence also connects a primary defect in invariant natural killer T (iNKT) cells to autoimmune disease development. However, exactly how this unconventional T cell subset is involved remains to be defined. Here, we identify a suppressive role for iNKT cells in a model where autoantibody production is triggered by an increased load of circulating apoptotic cells, resembling the situation in SLE patients. Absence or reduction of iNKT cells as well as absence of CD1d-expression on B cells, needed for direct iNKT-B cell interaction, leads to increased autoreactive B cell activation and symptoms of disease. The suppression mediated by the iNKT cells is observed before B cell entry into germinal centers and can be rescued by transferring iNKT cells to deficient mice. This links iNKT cells to handling of dying cells and identifies a novel peripheral tolerance checkpoint relevant for autoimmune disease. Thus, these observations connect two clinical observations in SLE patients previously considered to be unrelated and define a new target for immunotherapy.

Indexed as

AnimalsAntigens, CD1dApoptosisAutoimmune DiseasesB-LymphocytesCytokinesHumansLupus Erythematosus, SystemicLymphocyte ActivationLymphocyte DepletionMiceNatural Killer T-CellsSpleenAntigens, CD1dCytokines

Identifiers

PMID20439539
PMCPMC2867286
OpenAlexW2168813667

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.