Evidence map›Paper›PMID 25807036›Full record

ArticleKidney international2015

Gluten exacerbates IgA nephropathy in humanized mice through gliadin-CD89 interaction.

Christina Papista, Sebastian Lechner, Sanae Ben Mkaddem, Marie-Bénédicte LeStang, Lilia Abbad, Julie Bex-Coudrat, Evangéline Pillebout, Jonathan M Chemouny, Mathieu Jablonski, Martin Flamant and 5 more

Abstract read
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In one paragraph

Article in Kidney international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
6.8field-weighted citation impact, top 3% 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

55 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 citations in OpenAlex.

  1. Immunosuppressive therapy for IgA nephropathy in children.The Cochrane database of systematic reviews · 2024
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  9. Lessons from IgA Nephropathy Models.International journal of molecular sciences · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 4 institutions in 2 countries.

Christina Papista1] Institut National de la Santé et de la Recherche Médicale (INSERM) UMR 1149, Center for Research on Inflammation, Paris, France [2] Université Paris Diderot, Sorbonne Paris Cité, Paris, France [3] Inflamex Laboratory of Excellence, Faculté de Médecine Paris Diderot, Site Xavier Bichat, Paris, France [4] CNRS ERL8252, Paris, France.
Sebastian Lechner1] Institut National de la Santé et de la Recherche Médicale (INSERM) UMR 1149, Center for Research on Inflammation, Paris, France [2] Université Paris Diderot, Sorbonne Paris Cité, Paris, France [3] Inflamex Laboratory of Excellence, Faculté de Médecine Paris Diderot, Site Xavier Bichat, Paris, France [4] CNRS ERL8252, Paris, France.
Sanae Ben Mkaddem1] Institut National de la Santé et de la Recherche Médicale (INSERM) UMR 1149, Center for Research on Inflammation, Paris, France [2] Université Paris Diderot, Sorbonne Paris Cité, Paris, France [3] Inflamex Laboratory of Excellence, Faculté de Médecine Paris Diderot, Site Xavier Bichat, Paris, France [4] CNRS ERL8252, Paris, France.
Marie-Bénédicte LeStang1] Institut National de la Santé et de la Recherche Médicale (INSERM) UMR 1149, Center for Research on Inflammation, Paris, France [2] Université Paris Diderot, Sorbonne Paris Cité, Paris, France [3] Inflamex Laboratory of Excellence, Faculté de Médecine Paris Diderot, Site Xavier Bichat, Paris, France [4] CNRS ERL8252, Paris, France.
Lilia Abbad1] Institut National de la Santé et de la Recherche Médicale (INSERM) UMR 1149, Center for Research on Inflammation, Paris, France [2] Université Paris Diderot, Sorbonne Paris Cité, Paris, France [3] Inflamex Laboratory of Excellence, Faculté de Médecine Paris Diderot, Site Xavier Bichat, Paris, France [4] CNRS ERL8252, Paris, France.
Julie Bex-Coudrat1] Institut National de la Santé et de la Recherche Médicale (INSERM) UMR 1149, Center for Research on Inflammation, Paris, France [2] Université Paris Diderot, Sorbonne Paris Cité, Paris, France [3] Inflamex Laboratory of Excellence, Faculté de Médecine Paris Diderot, Site Xavier Bichat, Paris, France [4] CNRS ERL8252, Paris, France.
Evangéline PilleboutService de Néphrologie, Hôpital Saint-Louis, Paris, France.
Jonathan M Chemouny1] Institut National de la Santé et de la Recherche Médicale (INSERM) UMR 1149, Center for Research on Inflammation, Paris, France [2] Université Paris Diderot, Sorbonne Paris Cité, Paris, France [3] Inflamex Laboratory of Excellence, Faculté de Médecine Paris Diderot, Site Xavier Bichat, Paris, France [4] CNRS ERL8252, Paris, France.
Mathieu JablonskiNéphrologie, Paris, France.
Martin Flamant1] Institut National de la Santé et de la Recherche Médicale (INSERM) UMR 1149, Center for Research on Inflammation, Paris, France [2] Université Paris Diderot, Sorbonne Paris Cité, Paris, France [3] CNRS ERL8252, Paris, France [4] Exploration fonctionnelle, Paris, France.
Eric Daugas1] Institut National de la Santé et de la Recherche Médicale (INSERM) UMR 1149, Center for Research on Inflammation, Paris, France [2] Université Paris Diderot, Sorbonne Paris Cité, Paris, France [3] Inflamex Laboratory of Excellence, Faculté de Médecine Paris Diderot, Site Xavier Bichat, Paris, France [4] CNRS ERL8252, Paris, France [5] Néphrologie, Paris, France.
François Vrtovsnik1] Institut National de la Santé et de la Recherche Médicale (INSERM) UMR 1149, Center for Research on Inflammation, Paris, France [2] Université Paris Diderot, Sorbonne Paris Cité, Paris, France [3] Inflamex Laboratory of Excellence, Faculté de Médecine Paris Diderot, Site Xavier Bichat, Paris, France [4] CNRS ERL8252, Paris, France [5] Néphrologie, Paris, France.
Minas YiangouDepartment of Genetics, Development and Molecular Biology, School of Biology, Aristotle University of Thessaloniki, Thessaloniki, Greece.
Laureline Berthelot1] Institut National de la Santé et de la Recherche Médicale (INSERM) UMR 1149, Center for Research on Inflammation, Paris, France [2] Université Paris Diderot, Sorbonne Paris Cité, Paris, France [3] Inflamex Laboratory of Excellence, Faculté de Médecine Paris Diderot, Site Xavier Bichat, Paris, France [4] CNRS ERL8252, Paris, France.
Renato C Monteiro1] Institut National de la Santé et de la Recherche Médicale (INSERM) UMR 1149, Center for Research on Inflammation, Paris, France [2] Université Paris Diderot, Sorbonne Paris Cité, Paris, France [3] Inflamex Laboratory of Excellence, Faculté de Médecine Paris Diderot, Site Xavier Bichat, Paris, France [4] CNRS ERL8252, Paris, France [5] Immunologie, Assistance Publique de Paris, DHU Fire, Hôpital Bichat-Claude Bernard, Paris, France.
Centre National de la Recherche Scientifique · FRAristotle University of Thessaloniki · GRHôpital Saint-Louis · FRUniversité Claude Bernard Lyon 1 · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IgA1 complexes containing deglycosylated IgA1, IgG autoantibodies, and a soluble form of the IgA receptor (sCD89), are hallmarks of IgA nephropathy (IgAN). Food antigens, notably gluten, are associated with increased mucosal response and IgAN onset, but their implication in the pathology remains unknown. Here, an IgAN mouse model expressing human IgA1 and CD89 was used to examine the role of gluten in IgAN. Mice were given a gluten-free diet for three generations to produce gluten sensitivity, and then challenged for 30 days with a gluten diet. A gluten-free diet resulted in a decrease of mesangial IgA1 deposits, transferrin 1 receptor, and transglutaminase 2 expression, as well as hematuria. Mice on a gluten-free diet lacked IgA1-sCD89 complexes in serum and kidney eluates. Disease severity depended on gluten and CD89, as shown by reappearance of IgAN features in mice on a gluten diet and by direct binding of the gluten-subcomponent gliadin to sCD89. A gluten diet exacerbated intestinal IgA1 secretion, inflammation, and villous atrophy, and increased serum IgA1 anti-gliadin antibodies, which correlated with proteinuria in mice and patients. Moreover, early treatment of humanized mice with a gluten-free diet prevented mesangial IgA1 deposits and hematuria. Thus, gliadin-CD89 interaction may aggravate IgAN development through induction of IgA1-sCD89 complex formation and a mucosal immune response. Hence, early-stage treatment with a gluten-free diet could be beneficial to prevent disease.

Indexed as

AnimalsAntigens, CDAtrophyDiet, Gluten-FreeDisease Models, AnimalEnteritisGliadinGlomerulonephritis, IGAGlutensGTP-Binding ProteinsHematuriaImmunoglobulin AIntestinal MucosaMaleMiceProtein Glutamine gamma Glutamyltransferase 2Antigens, CDFc(alpha) receptorGliadinGlutensGTP-Binding ProteinsImmunoglobulin AProtein Glutamine gamma Glutamyltransferase 2Receptors, FcReceptors, TransferrinTfrc protein, mouseTransglutaminases

Identifiers

PMID25807036
OpenAlexW2075633094

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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.