Evidence map›Paper›PMID 26659093›Full record

ArticleImmunologic research2016

Th9 and Th22 immune response in young patients with type 1 diabetes.

Monika Ryba-Stanisławowska, Paulina Werner, Agnieszka Brandt, Małgorzata Myśliwiec, Jolanta Myśliwska

Abstract read
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Article in Immunologic research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

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  15. IL-10 Modulates Th17 Pathogenicity during Autoimmune Diseases.Journal of clinical & cellular immunology · 2016
    Article
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

5 authors.

Monika Ryba-StanisławowskaDepartment of Immunology, Medical University of Gdańsk, Dębinki 1, 80-211, Gdańsk, Poland. akinomab@gumed.edu.pl.ORCID 0000-0001-5784-267X
Paulina WernerDepartment of Immunology, Medical University of Gdańsk, Dębinki 1, 80-211, Gdańsk, Poland.
Agnieszka BrandtClinic of Pediatrics, Department of Diabetology and Endocrinology, Medical University of Gdańsk, 80-211, Gdańsk, Poland.
Małgorzata MyśliwiecClinic of Pediatrics, Department of Diabetology and Endocrinology, Medical University of Gdańsk, 80-211, Gdańsk, Poland.
Jolanta MyśliwskaDepartment of Immunology, Medical University of Gdańsk, Dębinki 1, 80-211, Gdańsk, Poland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Th17, Th22 and Th9 are recently discovered effector populations that may contribute to the pathogenesis of autoimmune and inflammatory diseases. The presented study aimed to investigate the link between Th22 and Th9 subsets in type 1 diabetes, as this disease involves different subsets of CD4+ T lymphocytes. The study groups consisted of 23 patients with type 1 diabetes and 11 healthy individuals. All subjects had CD4+IL-22 Th22 and CD4+IL-9 Th9 lymphocytes investigated by flow cytometry. In addition, the plasma concentrations of IL-22 as well as IL-9 were analyzed. Our study demonstrated that Th9 and Th22 cell counts as well as their plasma cytokines were upregulated in patients with type 1 and correlated with HbA1c and CRP values. Taking these all into account, one can conclude that Th22 and Th9 lymphocyte activities may contribute to chronic, low-level inflammation that is considered an integral part of type 1 diabetes.

Indexed as

AdolescentAge FactorsChildC-Reactive ProteinDiabetes Mellitus, Type 1FemaleGlycated HemoglobinHumansImmunity, CellularImmunophenotypingInterleukin-22Interleukin-9InterleukinsMaleTh17 CellsT-Lymphocyte SubsetsC-Reactive ProteinGlycated Hemoglobinhemoglobin A1c protein, humanInterleukin-22Interleukin-9InterleukinsIL-22IL-9Th22Th9Type 1 diabetes

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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.