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Subtyping of Type 1 Diabetes as Classified by Anti-GAD Antibody, IgE Levels, and Tyrosine kinase 2 (TYK2) Promoter Variant in the Japanese.
Mine, Keiichiro; Hirakawa, Kanako; Kondo, Shiori; Minami, Masae; Okada, Akira; Tsutsu, Nobutaka; Yokogawa, Yasushi; Hibio, Yumi; Kojima, Fumiko; Fujimoto, Shuji; Kurisaki, Hironori; Anzai, Keizo; Yoshikai, Yasunobu; Nagafuchi, Seiho.
Afiliación
  • Mine K; Division 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.
  • Hirakawa K; Department 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.
  • Kondo S; Matsuyama Red Cross Hospital, 1, Bunkyo-machi, Matsuyama-shi, Ehime, Japan. Electronic address: shiori@matsuyama.jrc.or.jp.
  • Minami M; Minami Masae Naika Clinic, 1-4-6, Heiwa, Minami-ku, Fukuoka, Japan. Electronic address: mmasaecl@ace.ocn.ne.jp.
  • Okada A; Okada Naika Clinic, 7-8-8, Hakozaki, Higashi-ku, Fukuoka, Japan. Electronic address: okada@okadaclinic.or.jp.
  • Tsutsu N; Department of Diabetes and Metabolism, Fukuoka Red Cross Hospital, 3-1-1, Minami-ku, Fukuoka, Japan. Electronic address: tsutsu26822@yahoo.co.jp.
  • Yokogawa Y; Yokogawa Naika Clinic, 5-7-7, Tenjin, Chuo-ku, Fukuoka, Japan. Electronic address: yssyokogawa@kjc.biglobe.ne.jp.
  • Hibio Y; Department 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.
  • Kojima F; Department 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.
  • Fujimoto S; Department 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.
  • Kurisaki H; Department 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.
  • Anzai K; Department of Hepatology, Diabetes and Endocrinology, Faculty of Medicine, Saga University, 5-1-1, Nabeshima, Saga, Japan. Electronic address: akeizo@cc.saga-u.ac.jp.
  • Yoshikai Y; Division 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.
  • Nagafuchi S; Department 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@m
EBioMedicine ; 23: 46-51, 2017 Sep.
Article en En | MEDLINE | ID: mdl-28826655
OBJECTIVE: Type 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 METHODS: We 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. RESULTS: T1D 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). INTERPRETATION: Anti-GAD Ab and IgE profiling helps classifying T1D into four groups that recognize variable pathogenic bases of T1D.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Autoanticuerpos / Variación Genética / Inmunoglobulina E / Regiones Promotoras Genéticas / Diabetes Mellitus Tipo 1 / TYK2 Quinasa Tipo de estudio: Etiology_studies Límite: Adolescent / Adult / Aged / Aged80 / Child / Female / Humans / Male / Middle aged País/Región como asunto: Asia Idioma: En Revista: EBioMedicine Año: 2017 Tipo del documento: Article Pais de publicación: Países Bajos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Autoanticuerpos / Variación Genética / Inmunoglobulina E / Regiones Promotoras Genéticas / Diabetes Mellitus Tipo 1 / TYK2 Quinasa Tipo de estudio: Etiology_studies Límite: Adolescent / Adult / Aged / Aged80 / Child / Female / Humans / Male / Middle aged País/Región como asunto: Asia Idioma: En Revista: EBioMedicine Año: 2017 Tipo del documento: Article Pais de publicación: Países Bajos