Evidence map›Paper›PMID 20398308›Full record

ArticleArthritis research & therapy2010

B cells from rheumatoid arthritis patients show important alterations in the expression of CD86 and FcgammaRIIb, which are modulated by anti-tumor necrosis factor therapy.

Diego Catalán, Octavio Aravena, Francisca Sabugo, Pamela Wurmann, Lilian Soto, Alexis M Kalergis, Miguel Cuchacovich, Juan C Aguillón, Millenium Nucleus on Immunology and Immunotherapy P-07-088-F

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.7field-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

28 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
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  4. Serum immunoglobulin and the threshold of Fc receptor-mediated immune activation.Biochimica et biophysica acta. General subjects · 2023
    Review
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  10. Memory B Cells and Response to Abatacept in Rheumatoid Arthritis.Clinical reviews in allergy & immunology · 2017
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Diego CatalánPrograma Disciplinario de Inmunología, Instituto de Ciencias Biomédicas (ICBM), Facultad de Medicina, Universidad de Chile, Avenida Independencia 1027, Santiago, Chile.
Octavio Aravena
Francisca Sabugo
Pamela Wurmann
Lilian Soto
Alexis M Kalergis
Miguel Cuchacovich
Juan C Aguillón
Millenium Nucleus on Immunology and Immunotherapy P-07-088-F
University of Chile · CLHospital Clínico de la Universidad de Chile · CLPontificia Universidad Católica de Chile · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionSeveral molecules help preserve peripheral B cell tolerance, but when altered, they may predispose to autoimmunity. This work studied the expression of the costimulatory molecule CD86 and the inhibitory receptor for IgG immune complexes FcgammaRIIb (CD32b), on B cells from rheumatoid arthritis (RA) patients, and the influence of anti-tumor necrosis factor (TNF) therapy.

methodsPeripheral B cells from 18 RA patients and 13 healthy donors were characterized using flow cytometry. Eleven patients who underwent a six-month adalimumab therapy were further assessed for phenotypic changes on their B cells.

resultsRA patients exhibited a high percentage of naïve and memory B cells expressing CD86. In contrast, expression of FcgammaRIIb was significantly reduced on RA memory B cells and plasmablasts as compared to healthy donors, probably due to downregulation of this receptor when differentiating from naïve to memory cells. These alterations on FcgammaRIIb were associated with high levels of anti-citrullinated vimentin autoantibodies. In addition, treatment with adalimumab normalized the expression of CD86 on memory B cells and reduced the expression of FcgammaRIIb, mainly on naïve B cells.

conclusionsOur findings show that peripheral B cells from RA patients have an altered expression of key molecules, such as CD86 and FcgammaRIIb. Because this latter receptor is required for feedback inhibition, a deficient expression might contribute to humoral autoimmune responses. Furthermore, these molecules are likely to be influenced by inflammatory factors, since they were modulated by TNF inhibition.

Indexed as

AdalimumabAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntirheumatic AgentsArthritis, RheumatoidAutoantibodiesB7-2 AntigenB-LymphocytesFemaleHumansJointsMiddle AgedPeptides, CyclicReceptors, IgGSeverity of Illness IndexVimentinAdalimumabAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntirheumatic AgentsAutoantibodiesB7-2 AntigenCD86 protein, humancyclic citrullinated peptideFCGR2B protein, humanPeptides, CyclicReceptors, IgGVimentin

Identifiers

PMID20398308
PMCPMC2888223
OpenAlexW2122716489

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.