Evidence map›Paper›PMID 20113367›Full record

ArticleImmunology2010

Early activation of invariant natural killer T cells in a rheumatoid arthritis model and application to disease treatment.

Aurore Miellot-Gafsou, Jérôme Biton, Elvire Bourgeois, André Herbelin, Marie-Christophe Boissier, Natacha Bessis

Open access · greenAbstract read
In one paragraph

Article in Immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-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

17 citing papers in PubMed, 35 citations in OpenAlex.

  1. Cellular therapies in rheumatic and musculoskeletal diseases.Journal of translational autoimmunity · 2025
    Review
  2. Article
  3. The iNKT Cell-Macrophage Axis in Homeostasis and Disease.International journal of molecular sciences · 2022
    Review
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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

6 authors at 4 institutions in 1 country.

Aurore Miellot-GafsouUniversity of Paris 13, Bobigny, France.
Jérôme Biton
Elvire Bourgeois
André Herbelin
Marie-Christophe Boissier
Natacha Bessis
Assistance Publique – Hôpitaux de Paris · FRUniversité Sorbonne Paris Nord · FRDélégation Paris 5 · FRUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Invariant NKT (iNKT) cells are a distinctive subtype of CD1d-restricted T cells involved in regulating autoimmunity and capable of producing various T helper type 1 (Th1), Th2 and Th17 cytokines. Activation of iNKT cells by their exogenous ligand alpha-galactosylceramide (alpha-GalCer) exerts therapeutic effects in autoimmune diseases such as rheumatoid arthritis (RA). However, the pathophysiological role of iNKT cells in RA, in the absence of exogenous stimulation, is incompletely understood. We investigated the potential pathophysiological effects of iNKT cells in mice with collagen-induced arthritis (CIA), a model of RA. We found that iNKT cells underwent activation only in the early phases of the disease (6 days post-induction). In the liver, but not the spleen or lymph nodes, this early activation led to the release of interleukins -4, -17A and -10 and of interferon-gamma; and an increased CD69 expression. Importantly, clinical and histological signs of arthritis were improved by the functional blockade of iNKT cells by a monoclonal antibody to CD1d at the early phase of the disease. This improvement was associated on day 6 post-induction with decreased expression of co-stimulatory molecules (CD80, CD86, CD40) on splenic dendritic cells and macrophages, whereas regulatory T-cell suppressive effects and proportions were not modified. Taken in concert, these findings suggest that iNKT cells are activated early in the course of CIA and contribute to the pathogenesis of arthritis. Therefore, iNKT-cell activation may be a valid treatment target in RA.

Indexed as

AnimalsAntibodies, MonoclonalAntigens, CDAntigens, CD1dAntigens, Differentiation, T-LymphocyteArthritis, ExperimentalArthritis, RheumatoidCD69 AntigensCollagenCytokinesGalactosylceramidesGene Expression RegulationHumansLectins, C-TypeLymphocyte ActivationMalealpha-galactosylceramideAntibodies, MonoclonalAntigens, CDAntigens, CD1dAntigens, Differentiation, T-LymphocyteCd1d1 protein, mouseCD69 AntigensCollagenCytokinesGalactosylceramidesLectins, C-Type

Identifiers

PMID20113367
PMCPMC2878473
OpenAlexW1489598575

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.