, Volume 41, Issue 10, pp 1227–1232

Ingested interferon α suppresses Type I diabetes in non-obese diabetic mice


  • S. A. Brod
    • Department of Neurology, University of Texas-Houston, Houston, Texas, USA
  • M. Malone
    • Department of Neurology, University of Texas-Houston, Houston, Texas, USA
  • S. Darcan
    • Division of Paediatric Endocrinology, Department of Paediatrics, University of Texas-Houston, Houston, Texas, USA
  • M. Papolla
    • Department of Pathology, University of South Alabama Medical Centre, Mobile, Alabama, USA
  • L. Nelson
    • Graduate School of Biomedical Sciences, University of Texas-Houston, Houston, Texas, USA

DOI: 10.1007/s001250051056

Cite this article as:
Brod, S., Malone, M., Darcan, S. et al. Diabetologia (1998) 41: 1227. doi:10.1007/s001250051056


Type I diabetes mellitus is a chronic disorder that results from autoimmune destruction of the insulin-producing pancreatic beta cell. The non- obese diabetic mouse is a model of the human autoimmune disease Type I diabetes [1–3]. We have previously shown that ingested type 1 interferon inhibits chronic relapsing experimental autoimmune encephalomyelitis and the adoptive transfer of experimental autoimmune encephalomyelites by T cells, and decreases both antigen-specific and mitogen-induced pro-inflammatory cytokine secretion in this disorder. We therefore tried to determine whether ingested murine interferon α inhibits insulinitis and suppresses Type I diabetes mellitus in non-obese diabetic mice. Murine interferon α, given daily, decreased islet inflammation and suppressed diabetes. It increased the concanavalin A and ionomycin plus myristic acid palmitic ester-induced production of interleukin 4 and 10 and interferon γ-secretion in spleen cells from treated mice. Adoptive transfer of unstimulated splenocytes secreting interleukin 4 and interleukin 10 from fed interferon α donors suppressed spontaneous diabetes mellitus in recipients. The protective effect of adoptively transferred unstimulated splenocytes shows the presence of ingested interferon α-activated regulatory splenic cell populations that may work via increased interleukin 4 or interleukin 10 production. Ingested interferon α administered during vulnerable periods in at-risk populations may potentially provide a continuous, convenient, non-toxic and effective treatment for Type I diabetes. [Diabetologia (1998) 41: 1227–1232]

Keywords Non-obese diabetic mouse ingested interferon α interleukin 4 interleukin 10 adoptive transfer

Copyright information

© Springer-Verlag Berlin Heidelberg 1998