Evidence map›Paper›PMID 37885889›Full record

ArticleFrontiers in immunology2023

MAIT cells altered phenotype and cytotoxicity in lupus patients are linked to renal disease severity and outcome.

Elena Litvinova, Carine Bounaix, Guillaume Hanouna, Jennifer Da Silva, Laura Noailles, Lucie Beaudoin, Michael Padden, Nessrine Bellamri, Agnès Lehuen, Eric Daugas and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

14 citing papers in PubMed, 14 citations in OpenAlex.

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  4. Mucosal-Associated Invariant T Cells in Rheumatic Diseases.Arthritis & rheumatology (Hoboken, N.J.) · 2026
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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

12 authors at 7 institutions in 1 country.

Elena LitvinovaService d'Immunologie, Hôpital Bichat-Claude Bernard, Paris, France.
Carine BounaixUniversité Paris Cité, Centre de Recherche sur l'Inflammation Institut national de la santé et de la recherche médicale (INSERM) Unité Mixte de Recherche (UMR)1149 & Centre national de la recherche scientifique (CNRS) équipe mixte de recherche (EMR)8252, Inflamex Laboratory of Excellence, Paris, France.
Guillaume HanounaService de Néphrologie, Assistance publique - Hôpitaux de Paris (AP-HP), Hôpital Bichat-Claude Bernard, Paris, France.
Jennifer Da SilvaUniversité Paris Cité, Centre de Recherche sur l'Inflammation Institut national de la santé et de la recherche médicale (INSERM) Unité Mixte de Recherche (UMR)1149 & Centre national de la recherche scientifique (CNRS) équipe mixte de recherche (EMR)8252, Inflamex Laboratory of Excellence, Paris, France.
Laura NoaillesUniversité Paris Cité, Centre de Recherche sur l'Inflammation Institut national de la santé et de la recherche médicale (INSERM) Unité Mixte de Recherche (UMR)1149 & Centre national de la recherche scientifique (CNRS) équipe mixte de recherche (EMR)8252, Inflamex Laboratory of Excellence, Paris, France.
Lucie BeaudoinUniversité de Paris, Institut Cochin, Institut national de la santé et de la recherche médicale (INSERM) U1016, Centre national de la recherche scientifique (CNRS) Unité Mixte de Recherche (UMR) 8104, Inflamex Laboratory of Excellence, Paris, France.
Michael PaddenService de Néphrologie, Assistance publique - Hôpitaux de Paris (AP-HP), Hôpital Bichat-Claude Bernard, Paris, France.
Nessrine BellamriUniversité Paris Cité, Centre de Recherche sur l'Inflammation Institut national de la santé et de la recherche médicale (INSERM) Unité Mixte de Recherche (UMR)1149 & Centre national de la recherche scientifique (CNRS) équipe mixte de recherche (EMR)8252, Inflamex Laboratory of Excellence, Paris, France.
Agnès LehuenUniversité de Paris, Institut Cochin, Institut national de la santé et de la recherche médicale (INSERM) U1016, Centre national de la recherche scientifique (CNRS) Unité Mixte de Recherche (UMR) 8104, Inflamex Laboratory of Excellence, Paris, France.
Eric DaugasUniversité Paris Cité, Centre de Recherche sur l'Inflammation Institut national de la santé et de la recherche médicale (INSERM) Unité Mixte de Recherche (UMR)1149 & Centre national de la recherche scientifique (CNRS) équipe mixte de recherche (EMR)8252, Inflamex Laboratory of Excellence, Paris, France.
Renato C MonteiroService d'Immunologie, Hôpital Bichat-Claude Bernard, Paris, France.
Héloïse FlamentService d'Immunologie, Hôpital Bichat-Claude Bernard, Paris, France.
Centre National de la Recherche Scientifique · FRInserm · FRHôpital Bichat-Claude-Bernard · FRAssistance Publique – Hôpitaux de Paris · FRInstitut Cochin · FRUniversité Claude Bernard Lyon 1 · FRUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Systemic lupus erythematosus (SLE) is an autoimmune disease in which circulating immune complexes can cause different types of glomerulonephritis, according to immune deposits and to the type of glomerular cell injury. Proliferative lesions represent the most severe form of lupus nephritis (LN) and often lead to kidney failure and death. Mucosal-associated invariant T (MAIT) cells are a subset of innate-like T cells that recognize microbial-derived ligands from the riboflavin synthesis pathway. Although abundant in peripheral blood, MAIT cells are enriched in mucosal and inflamed tissues. While previous studies have reported concordant results concerning lower MAIT cell frequencies in the blood of SLE patients, no information is known about MAIT cell function and LN severity and outcome. Methods: In the current study, we analyzed the baseline phenotype and function of peripheral blood MAIT cells by flow cytometry in 26 patients with LN and in a control group of 16 healthy individuals. Results: We observe that MAIT cell frequencies are markedly reduced in blood of LN patients. MAIT cells from patients have an altered phenotype in terms of migration, proliferation and differentiation markers, notably in most severe forms of LN. Frequencies of PMA/ionomycin stimulated MAIT cells secreting effector molecules, such as proinflammatory IL-17 and cytotoxic protein granzyme B, are higher in LN patients. Patients undergoing a complete renal remission after immunosuppressive therapy had higher MAIT cell frequency, lower expression of proliferation marker Ki-67 and granzyme B (GzB) at inclusion. Remarkably, GzB production defines a predictive model for complete remission. Discussion: We report here that blood MAIT cells display proinflammatory and cytotoxic function in severe lupus nephritis which may play a pathogenesis role, but without association with systemic lupus activity. Finally, low cytotoxic profile of MAIT cells may represent a promising prognostic factor of lupus nephritis remission one year after induction therapy.

Indexed as

Lupus Erythematosus, SystemicLupus NephritisMucosal-Associated Invariant T CellsGranzymesHumansPatient AcuityPhenotypeGranzymesactivationgranzyme Blupus nephritisMAIT cellprognosis markers

Identifiers

PMID37885889
PMCPMC10598677
OpenAlexW4387478010

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Registered trials

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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.