Evidence map›Paper›PMID 28826655›Full record

ArticleEBioMedicine2017

Subtyping of Type 1 Diabetes as Classified by Anti-GAD Antibody, IgE Levels, and Tyrosine kinase 2 (TYK2) Promoter Variant in the Japanese.

Keiichiro Mine, Kanako Hirakawa, Shiori Kondo, Masae Minami, Akira Okada, Nobutaka Tsutsu, Yasushi Yokogawa, Yumi Hibio, Fumiko Kojima, Shuji Fujimoto and 5 more

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Article in EBioMedicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.5field-weighted citation impact, top 15% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Quantitative temporal analysis of pancreatic islet T lymphocyte and macrophage infiltration heralded by serum IgE in congenic BioBreeding (BB) Gimap5Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 7 institutions in 1 country.

Keiichiro MineDivision of Host Defense, Medical Institute of Bioregulation, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka, Japan. Electronic address: k_mine@bioreg.kyushu-u.ac.jp.
Kanako HirakawaDepartment of Medical Science and Technology, Graduate School of Medical Sciences, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka, Japan. Electronic address: wish_on_a_star@live.jp.
Shiori KondoMatsuyama Red Cross Hospital, 1, Bunkyo-machi, Matsuyama-shi, Ehime, Japan. Electronic address: shiori@matsuyama.jrc.or.jp.
Masae MinamiMinami Masae Naika Clinic, 1-4-6, Heiwa, Minami-ku, Fukuoka, Japan. Electronic address: mmasaecl@ace.ocn.ne.jp.
Akira OkadaOkada Naika Clinic, 7-8-8, Hakozaki, Higashi-ku, Fukuoka, Japan. Electronic address: okada@okadaclinic.or.jp.
Nobutaka TsutsuDepartment of Diabetes and Metabolism, Fukuoka Red Cross Hospital, 3-1-1, Minami-ku, Fukuoka, Japan. Electronic address: tsutsu26822@yahoo.co.jp.
Yasushi YokogawaYokogawa Naika Clinic, 5-7-7, Tenjin, Chuo-ku, Fukuoka, Japan. Electronic address: yssyokogawa@kjc.biglobe.ne.jp.
Yumi HibioDepartment of Medical Science and Technology, Graduate School of Medical Sciences, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka, Japan; Center for Clinical Laboratory Examination, Fukuoka Medical Association, 1-6-9, Sawara-ku, Fukuoka, Japan. Electronic address: yumi30829@yahoo.co.jp.
Fumiko KojimaDepartment of Medical Science and Technology, Graduate School of Medical Sciences, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka, Japan. Electronic address: fumikoji@med.kyushu-u.ac.jp.
Shuji FujimotoDepartment of Medical Science and Technology, Graduate School of Medical Sciences, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka, Japan. Electronic address: shuuji@med.kyushu-u.ac.jp.
Hironori KurisakiDepartment of Medical Science and Technology, Graduate School of Medical Sciences, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka, Japan. Electronic address: kurisaki@med.kyushu-u.ac.jp.
Keizo AnzaiDepartment of Hepatology, Diabetes and Endocrinology, Faculty of Medicine, Saga University, 5-1-1, Nabeshima, Saga, Japan. Electronic address: akeizo@cc.saga-u.ac.jp.
Yasunobu YoshikaiDivision of Host Defense, Medical Institute of Bioregulation, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka, Japan. Electronic address: yoshikai.yasunobu.056@m.kyushu-u.ac.jp.
Seiho NagafuchiDepartment of Medical Science and Technology, Graduate School of Medical Sciences, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka, Japan; Department of Hepatology, Diabetes and Endocrinology, Faculty of Medicine, Saga University, 5-1-1, Nabeshima, Saga, Japan. Electronic address: nagafu_s@med.kyushu-u.ac.jp.
West Japan Pathogenesis of Diabetes Study Group
Kyushu University · JPFukuoka Hospital · JPJapanese Red Cross Fukuoka Hospital · JPMatsuyama Red Cross Hospital · JPOki Electric Industry (Japan) · JPSaga University · JPYokogawa Electric (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveType 1 diabetes (T1D) is known to be caused by Th1 cell-dependent autoimmunity. Recently, we reported that TYK2 promoter variant serves as a putative virus-induced diabetes susceptibility gene associated with deteriorated interferon-dependent antiviral response. TYK2 is also related to HIES, that is, Th2 cell-dependent. Therefore, TYK2 promoter variant may be also associated with the pathogenesis of T1D, modulating Th1/Th2 balance. RESEARCH DESIGN AND

methodsWe assessed the association between anti- GAD Ab, IgE levels, and TYK2 promoter variant among 313 T1D patients, 184 T2D patients, and 264 YH controls in the Japanese.

resultsT1D patients had elevated IgE (median, 56.7U/ml; p<0.0001) compared with T2D patients (22.5U/ml) and controls (43.3U/ml). Contrary to our expectations, there was no correlation between TYK2 promoter variant and IgE levels. We found that T1D could be subtyped as four groups based on anti-GAD Ab and IgE profile: Subtype 1, anti-GAD Ab positive and non-elevated IgE (47.0%); Subtype 2, anti-GAD Ab negative and non-elevated IgE (35.1%); Subtype 3, anti-GAD Ab positive and elevated IgE (10.9%); and Subtype 4, anti-GAD Ab negative and elevated IgE (7.0%). In Subtype 2, a significantly higher incidence was observed in T1D cases carrying the TYK2 promoter variant (OR, 2.60; 95%CI, 1.03-6.97; p=0.032), and also showing a flu-like syndrome at diabetes onset (OR, 2.34; 95%CI, 1.27-4.35; p=0.003).

interpretationAnti-GAD Ab and IgE profiling helps classifying T1D into four groups that recognize variable pathogenic bases of T1D.

Indexed as

Genetic VariationPromoter Regions, GeneticAdolescentAdultAgedAged, 80 and overAutoantibodiesAutoantigensAutoimmunityChildDiabetes Mellitus, Type 1Diabetes Mellitus, Type 2Disease SusceptibilityFemaleGenotypeHumansAutoantibodiesAutoantigensImmunoglobulin ETYK2 KinaseAnti-GADIgETh1/Th2Type 1 diabetes (T1D)Tyrosine kinase 2 (TYK2)Virus

Identifiers

PMID28826655
PMCPMC5605380
OpenAlexW2744907148

What OpenQuestion holds

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LicenceCC BY
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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.