Evidence map›Paper›PMID 26271387›Full record

ArticleJournal of clinical immunology2015

Paradoxical Expansion of Th1 and Th17 Lymphocytes in Rheumatoid Arthritis Following Infliximab Treatment: a Possible Explanation for a Lack of Clinical Response.

Rossella Talotta, Angela Berzi, Fabiola Atzeni, Alberto Batticciotto, Mario Clerici, Piercarlo Sarzi-Puttini, Daria Trabattoni

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Journal of clinical immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
  2. Th17 and CD24Arthritis research & therapy · 2017
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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

7 authors at 3 institutions in 1 country.

Rossella TalottaRheumatology Unit, Department of Internal Medicine, L. Sacco University Hospital, Milan, Italy.
Angela BerziL. Sacco Department of Biomedical and Clinical Sciences, University of Milan, Via GB Grassi 74, 20157, Milan, Italy.
Fabiola AtzeniRheumatology Unit, Department of Internal Medicine, L. Sacco University Hospital, Milan, Italy.
Alberto BatticciottoRheumatology Unit, Department of Internal Medicine, L. Sacco University Hospital, Milan, Italy.
Mario ClericiDepartment of Physiopathology and Transplantation, University of Milan, Milan, Italy.
Piercarlo Sarzi-PuttiniRheumatology Unit, Department of Internal Medicine, L. Sacco University Hospital, Milan, Italy.
Daria TrabattoniL. Sacco Department of Biomedical and Clinical Sciences, University of Milan, Via GB Grassi 74, 20157, Milan, Italy. daria.trabattoni@unimi.it.
Luigi Sacco Hospital · ITDon Carlo Gnocchi Foundation · ITUniversity of Milan · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThe immunogenicity of anti-TNF-α drugs may affect their safety and efficacy. Infliximab (IFX), a chimeric monoclonal antibody, induces antibody formation in up to 60% of cases. Some studies have suggested the involvement of a Th1 response to TNFα blockers following immunization, but the triggering of Th17 responses has never been reported. The aim of this study is to investigate whether the immunogenicity of IFX affects the Th1, Th17 and Treg compartments in rheumatoid arthritis (RA) patients failing IFX therapy, and verify whether this may be responsible for treatment failure.

methodsThe study involved 55 patients with RA (15 treatment-naïve patients; 20 IFX responders; 20 IFX non-responders) and 10 healthy controls. PBMCs were cultured in the presence/absence of IFX, and the variations in the percentage of Th1, Th17 and Treg lymphocytes following IFX treatment were analysed.

resultsIFX-specific Th1 and Th17 responses and an increase in IL-21 production were observed in patients failing IFX (p < 0.01, p < 0.05, and p < 0.01 respectively). In contrast, IFX incubation reduced significantly Th1 and Th17 responses and IL-21 production (p < 0.05) in successfully-treated subjects, but did not affect these responses in healthy controls or treatment-naïve patients.

conclusionsRA patients may have impaired peripheral tolerance, which could favour the development of an aberrant immunological response to biological drugs. The loss of therapeutic effectiveness of IFX and the onset of adverse events may be due to a paradoxical activation of Th17 or Th1 lymphocytes following sensitisation, thus worsening the patients' inflammatory status.

Indexed as

AdultAgedArthritis, RheumatoidCell ProliferationCells, CulturedFemaleHumansInfliximabInterleukin-21InterleukinsMaleMiddle AgedTh17 CellsTh1 CellsT-Lymphocytes, RegulatoryTreatment FailureInfliximabInterleukin-21InterleukinsTumor Necrosis Factor-alphaimmunogenicityinfliximabRheumatoid arthritisTh17 lymphocytesTh1 lymphocytes

Identifiers

PMID26271387
OpenAlexW1162001259

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.