Modulation of nuclear factor-κB activity can influence the susceptibility to systemic lupus erythematosus

Alexis M. Kalergis, Mirentxu I. Iruretagoyena, Magaly J. Barrientos, Pablo A. González, Andres A. Herrada, Eduardo D. Leiva, Miguel A. Gutiérrez, Claudia A. Riedel, Susan M. Bueno, Sergio H. Jacobelli

Resultado de la investigación: Contribución a una revistaArtículorevisión exhaustiva

47 Citas (Scopus)


Autoimmune diseases, such as systemic lupus erythematosus (SLE), result from deficiencies in self-antigen tolerance processes, which require regulated dendritic cell (DC) function. In this study we evaluated the phenotype of DCs during the onset of SLE in a mouse model, in which deletion of the inhibitory receptor FcβRIIb leads to the production of anti-nuclear antibodies and glomerulonephritis. Splenic DCs from FcβRIIb-deficient mice suffering from SLE showed increased expression of co-stimulatory molecules. Furthermore, diseased mice showed an altered function of the nuclear factor-κB (NF-κB) transcription factor, which is involved in DC maturation. Compared with healthy animals, expression of the inhibitory molecule IκB-α was significantly decreased in mice suffering from SLE. Consistently, pharmacological inhibition of NF-κB activity in FcβRIIb-deficient mice led to reduced susceptibility to SLE and prevented symptoms, such as anti-nuclear antibodies and kidney damage. Our data suggest that the occurrence of SLE is significantly influenced by alterations of NF-κB function, which can be considered as a new therapeutic target for this disease.

Idioma originalInglés
Páginas (desde-hasta)e306-e314
N.º1 PART 2
EstadoPublicada - sep 2009

Áreas temáticas de ASJC Scopus

  • Inmulogía y alergología
  • Inmunología


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