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

SA Brod, M Malone, S Darcan, M Papolla, L Nelson - Diabetologia, 1998 - Springer
SA Brod, M Malone, S Darcan, M Papolla, L Nelson
Diabetologia, 1998Springer
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 …
Summary
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]
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