Evidence map›Paper›PMID 26353115›Full record

ArticlePloS one2015

Constitutive STAT3 Phosphorylation in Circulating CD4+ T Lymphocytes Associates with Disease Activity and Treatment Response in Recent-Onset Rheumatoid Arthritis.

Krista Kuuliala, Antti Kuuliala, Riitta Koivuniemi, Suvi Oksanen, Mari Hämäläinen, Eeva Moilanen, Hannu Kautiainen, Marjatta Leirisalo-Repo, Heikki Repo

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 13% 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, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

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  8. Biochanin A impedes STAT3 activation by upregulating p38δ MAPK phosphorylation in IL-6-stimulated macrophages.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020
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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

9 authors at 3 institutions in 1 country.

Krista KuulialaBacteriology and Immunology, Helsinki University Hospital and University of Helsinki, Helsinki, Finland.
Antti KuulialaBacteriology and Immunology, Helsinki University Hospital and University of Helsinki, Helsinki, Finland.
Riitta KoivuniemiRheumatology, Helsinki University Hospital and University of Helsinki, Helsinki, Finland.
Suvi OksanenBacteriology and Immunology, Helsinki University Hospital and University of Helsinki, Helsinki, Finland.
Mari HämäläinenImmunopharmacology Research Group, University of Tampere School of Medicine and Tampere University Hospital, Tampere, Finland.
Eeva MoilanenImmunopharmacology Research Group, University of Tampere School of Medicine and Tampere University Hospital, Tampere, Finland.
Hannu KautiainenPrimary Health Care, Helsinki University Hospital and University of Helsinki, Helsinki, Finland; General Practice, Helsinki University Hospital and University of Helsinki, Helsinki, Finland; Unit of Primary Health Care, Kuopio University Hospital, Kuopio, Finland.
Marjatta Leirisalo-RepoBacteriology and Immunology, Helsinki University Hospital and University of Helsinki, Helsinki, Finland; Rheumatology, Helsinki University Hospital and University of Helsinki, Helsinki, Finland.
Heikki RepoBacteriology and Immunology, Helsinki University Hospital and University of Helsinki, Helsinki, Finland.
Helsinki University Hospital · FITampere University · FIUniversity of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of the present study was to examine constitutive signal transducer and activator of transcription 3 (STAT3) phosphorylation in circulating leukocytes as a candidate biomarker in rheumatoid arthritis (RA). 25 patients with recent-onset, untreated RA provided samples for whole blood flow cytometric determination of intracellular STAT3 phosphorylation, expressed as relative fluorescence units. The occurrence of constitutive STAT3 phosphorylation was evaluated by determining proportion of STAT3-phosphorylated cells among different leukocyte subtypes. Plasma levels of interleukin (IL)-6, IL-17 and IL-21 were measured by immunoassay, radiographs of hands and feet were examined and disease activity score (DAS28) was determined. Biomarkers were restudied and treatment response (according to European League Against Rheumatism) was determined after 12 months of treatment with disease-modifying antirheumatic drugs. At baseline, constitutive phosphorylation of STAT3 occurred in CD4+ T cells of 14 (56%) patients, CD8+ T cells of 13 (52%) patients, in CD19+ B cells of 7 (28%) patients, and in CD14+ monocytes of 12 (48%) patients. STAT3 phosphorylation levels of CD4+ T cells associated with DAS28, and those of all leukocyte subtypes studied associated with erosive disease. The presence of constitutive STAT3 phosphorylation in CD4+ T lymphocytes, pSTAT3 fluorescence intensity of CD4+ and CD8+ T cells and C-reactive protein (CRP) levels at baseline associated with good treatment response. In conclusion, constitutive STAT3 phosphorylation in circulating CD4+ T cells is common in recent-onset untreated RA and associates with good treatment response in patients characterized by high disease activity and the presence of systemic inflammation.

Indexed as

AdultAntirheumatic AgentsArthritis, RheumatoidB-LymphocytesCD4-Positive T-LymphocytesCytokinesFemaleHumansLeukocytesMaleMiddle AgedMonocytesPhosphorylationSTAT3 Transcription FactorT-Lymphocytes, CytotoxicAntirheumatic AgentsCytokinesSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID26353115
PMCPMC4564221
OpenAlexW2164291698

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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.