Short-Term High Expression of Interferon-Alpha Modulates Progression of Type 1 Diabetes in NOD Mice.
- Author:
Mi Kyoung PARK
1
;
Su Yeong SEO
;
Sook Hee HONG
;
Hye Jin KIM
;
Eun Jin PARK
;
Duk Kyu KIM
;
Hye Jeong LEE
Author Information
1. Department of Internal Medicine, Dong-A University College of Medicine, Busan 602-714, Korea.
- Publication Type:Original Article
- Keywords:
IFN-alpha;
T1D;
Adenoviral-mediated delivery;
Immunomodulation
- MeSH:
Animals;
Autoimmune Diseases;
Autoimmunity;
Cytokines;
Diabetes Mellitus, Type 1;
Immunomodulation;
Interferon-alpha*;
Interleukin-12;
Interleukin-4;
Interleukin-6;
Islets of Langerhans;
Mice;
Mice, Inbred NOD*;
Th2 Cells
- From:The Korean Journal of Physiology and Pharmacology
2006;10(1):39-44
- CountryRepublic of Korea
- Language:English
-
Abstract:
Type I diabetes (T1D) is an organ-specific autoimmune disease caused by the T cell-mediated destruction of the insulin-producing beta cells in the pancreatic islets. The onset of T1D is the consequence of a progressive destruction of islet beta cells mediated by an imbalance between effector CD4+ T helper (Th)1 and regulatory CD4+ Th2 cell function. Since interferon-alpha (IFN-alpha) has been known to modulate immune function and autoimmunity, we investigated whether administration of adenoviral-mediated IFN-alpha gene would inhibit the diabetic process in NOD mice. The development of diabetes was significantly inhibited by a single injection of adenoviral-mediated IFN-alpha gene before 8 weeks of age. Next, we examined the hypothesis that Th2-type cytokines are associated with host protection against autoimmune diabetes, whereas Th1-type cytokines are associated with pathogenesis of T1D. The expression of IFN-alpha induced increase of serum IL-4 and IL-6 (Th2 cytokines) levels and decrease of serum IL-12 and IFN-gamma (Th1 cytokines) levels. Therefore, overexpression of IFN-alpha by adenoviral-mediated delivery provides modulation of pathogenic progression and protection of NOD mice from T1D.
