1alpha,25-dihydroxyvitamin D3 induces an autoantigen-specific T-helper 1/T-helper 2 immune shift in NOD mice immunized with GAD65 (p524-543).

• DOI: 10.2337/diabetes.49.8.1301
• Publication Date: 2007-03-06T19:04:22Z
• Authors: L Overbergh; B Decallonne; M Waer; O Rutgeerts; D Valckx; K M Casteels; J Laureys; R Bouillon; C Mathieu
• Keywords: NOD mice

Prevention of type 1 diabetes in NOD mice by 1,25-dihydroxyvitamin D3 [1alpha,25(OH)2D3] is accompanied a T-helper (Th) 1/Th2 cytokine shift the pancreas. The aim this study was to investigate whether immune also occurs outside pancreas and it limited autoantigen-specific responses. treated with 1alpha,25(OH)2D3 (5 microg/kg every 2 days) or control vehicle were immunized GAD65 (p524-543) ovalbumin (OVA) rear footpads. First, we examined T-cell proliferation production (via enzyme-linked immunosorbent assay) draining lymph node cells vitro without peptide rechallenge. Although no differences measured between 1alpha,25(OH)2D3-treated after rechallenge, marked secretion profile seen mice: interleukin-4 increased (37 +/- 5 vs. 21 12 pg/ml controls, P < 0.005), whereas gamma-interferon levels decreased (6 3 9 ng/ml 0.05). This absent OVA-primed mice. Second, profiles reverse transcriptase-polymerase chain reaction popliteal nodes at different time points priming OVA vivo. A Th1/Th2 occurred vivo GAD65. Again, immunization. Finally, rechallenge panel autoantigens (GAD65, heat shock protein 65, insulin B-chain) antigens (OVA, keyhole limpet hemocyanine, myelin proteolipid protein, tetanus toxin) confirmed autoantigen-injected but not antigen-injected In conclusion, deviation induced can be peripheral system pancreatic autoantigens.