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2. Oral administration of the immunodominant B-chain of insulin reduces diabetes in a co-transfer model of diabetes in the NOD mouse and is associated with a switch from Th1 to Th2 cytokines. Polanski M, Melican NS, Zhang J, Weiner HL. J Autoimmun; 1997 Aug; 10(4):339-46. PubMed ID: 9237797 [Abstract] [Full Text] [Related]
3. Deviation of pancreas-infiltrating cells to Th2 by interleukin-12 antagonist administration inhibits autoimmune diabetes. Trembleau S, Penna G, Gregori S, Gately MK, Adorini L. Eur J Immunol; 1997 Sep; 27(9):2330-9. PubMed ID: 9341777 [Abstract] [Full Text] [Related]
4. Regulatory Th2-type T cell lines against insulin and GAD peptides derived from orally- and nasally-treated NOD mice suppress diabetes. Maron R, Melican NS, Weiner HL. J Autoimmun; 1999 Jun; 12(4):251-8. PubMed ID: 10330296 [Abstract] [Full Text] [Related]
12. B lymphocytes are crucial antigen-presenting cells in the pathogenic autoimmune response to GAD65 antigen in nonobese diabetic mice. Falcone M, Lee J, Patstone G, Yeung B, Sarvetnick N. J Immunol; 1998 Aug 01; 161(3):1163-8. PubMed ID: 9686575 [Abstract] [Full Text] [Related]
20. Induction of glutamic acid decarboxylase 65-specific Th2 cells and suppression of autoimmune diabetes at late stages of disease is epitope dependent. Tisch R, Wang B, Serreze DV. J Immunol; 1999 Aug 01; 163(3):1178-87. PubMed ID: 10415012 [Abstract] [Full Text] [Related] Page: [Next] [New Search]