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The effect of interleukin-22 treatment on autoimmune diabetes in the NOD mouse.
Borg, Danielle J; Wang, Ran; Murray, Lydia; Tong, Hui; Steptoe, Raymond J; McGuckin, Michael A; Hasnain, Sumaira Z.
Afiliación
  • Borg DJ; Inflammatory Diseases Biology and Therapeutics, Mater Research Institute - The University of Queensland, Translational Research Institute, Level 4/37 Kent Street, Woolloongabba, Brisbane, QLD, 4102, Australia.
  • Wang R; Inflammatory Diseases Biology and Therapeutics, Mater Research Institute - The University of Queensland, Translational Research Institute, Level 4/37 Kent Street, Woolloongabba, Brisbane, QLD, 4102, Australia.
  • Murray L; Inflammatory Diseases Biology and Therapeutics, Mater Research Institute - The University of Queensland, Translational Research Institute, Level 4/37 Kent Street, Woolloongabba, Brisbane, QLD, 4102, Australia.
  • Tong H; Inflammatory Diseases Biology and Therapeutics, Mater Research Institute - The University of Queensland, Translational Research Institute, Level 4/37 Kent Street, Woolloongabba, Brisbane, QLD, 4102, Australia.
  • Steptoe RJ; Tolerance and Autoimmunity Group, University of Queensland Diamantina Institute, Translational Research Institute, Brisbane, QLD, Australia.
  • McGuckin MA; Inflammatory Diseases Biology and Therapeutics, Mater Research Institute - The University of Queensland, Translational Research Institute, Level 4/37 Kent Street, Woolloongabba, Brisbane, QLD, 4102, Australia.
  • Hasnain SZ; Inflammatory Diseases Biology and Therapeutics, Mater Research Institute - The University of Queensland, Translational Research Institute, Level 4/37 Kent Street, Woolloongabba, Brisbane, QLD, 4102, Australia. sumaira.hasnain@mater.uq.edu.au.
Diabetologia ; 60(11): 2256-2261, 2017 Nov.
Article en En | MEDLINE | ID: mdl-28779211
AIMS/HYPOTHESIS: The aim of this study was to determine whether therapy with the cytokine IL-22 could be used to prevent the development of, or treat, autoimmune diabetes in the NOD mouse. METHODS: Six-week-old NOD mice were administered bi-weekly either recombinant mouse IL-22 (200 ng/g) or PBS (vehicle control) intraperitoneally until overt diabetes was diagnosed as two consecutive measurements of non-fasting blood glucose ≥ 11 mmol/l. At this time, NOD mice in the control arm were treated with LinBit insulin pellets and randomised to bi-weekly therapeutic injections of either PBS or IL-22 (200 ng/g) and followed until overt diabetes was diagnosed, as defined above. RESULTS: IL-22 therapy did not delay the onset of diabetes in comparison with the vehicle-treated mice. We did not observe an improvement in islet area, glycaemic control, beta cell residual function, endoplasmic reticulum stress, insulitis or macrophage and neutrophil infiltration as determined by non-fasting blood glucose, C-peptide and histological scoring. Therapeutic administration of IL-22 did not reduce circulating lipopolysaccharide, a marker of impaired gut mucosal integrity. CONCLUSIONS/INTERPRETATION: Our study suggests that, at this dosing regimen introduced either prior to overt diabetes or at diagnosis of diabetes, recombinant mouse IL-22 therapy cannot prevent autoimmune diabetes, or prolong the honeymoon period in the NOD mouse.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Interleucinas / Diabetes Mellitus Tipo 1 Límite: Animals Idioma: En Revista: Diabetologia Año: 2017 Tipo del documento: Article País de afiliación: Australia Pais de publicación: Alemania

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Interleucinas / Diabetes Mellitus Tipo 1 Límite: Animals Idioma: En Revista: Diabetologia Año: 2017 Tipo del documento: Article País de afiliación: Australia Pais de publicación: Alemania