Short-Term High Expression of Interferon-Alpha Modulates Progression of Type 1 Diabetes in NOD Mice
The Korean Journal of Physiology and Pharmacology
;
: 39-44, 2006.
Artículo
en Inglés
| WPRIM
| ID: wpr-728402
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.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Enfermedades Autoinmunes
/
Autoinmunidad
/
Citocinas
/
Islotes Pancreáticos
/
Interleucina-4
/
Interleucina-6
/
Ratones Endogámicos NOD
/
Interferón-alfa
/
Células Th2
/
Interleucina-12
Límite:
Animales
Idioma:
Inglés
Revista:
The Korean Journal of Physiology and Pharmacology
Año:
2006
Tipo del documento:
Artículo
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