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

S. A. Brod, M. Malone, S. Darcan, M. Papolla, L. Nelson

Research output: Contribution to journalArticlepeer-review

38 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)1227-1232
Number of pages6
Issue number10
StatePublished - 1998
Externally publishedYes


  • Adoptive transfer
  • Ingested interferon α
  • Interleukin 10
  • Interleukin 4
  • Non-obese diabetic mouse

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism


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