The Nuclear IκB Family Protein IκBNS Influences the Susceptibility to Experimental Autoimmune Encephalomyelitis in a Murine Model

نویسندگان

  • Shuhei Kobayashi
  • Akira Hara
  • Takayuki Isagawa
  • Ichiro Manabe
  • Kiyoshi Takeda
  • Takashi MaruYama
چکیده

The nuclear IκB family protein IκBNS is expressed in T cells and plays an important role in Interferon (IFN)-γ and Interleukin (IL)-2 production. IκB-ζ, the most similar homolog of IκBNS, plays an important role in the generation of T helper (Th)17 cells in cooperation with RORγt, a master regulator of Th17 cells. Thus, IκB-ζ deficient mice are resistant to Th17-dependent experimental autoimmune encephalomyelitis (EAE). However, IκB-ζ deficient mice develop the autoimmune-like Sjögren syndrome with aging. Here we found that IκBNS-deficient (Nfkbid-/-) mice show resistance against developing Th17-dependent EAE. We found that Nfkbid-/- T cells have decreased expression of IL-17-related genes and RORγt in response to Transforming Growth Factor (TGF)-β1 and IL-6 stimulation. Thus, IκBNS plays a pivotal role in the generation of Th17 cells and in the control of Th17-dependent EAE.

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عنوان ژورنال:

دوره 9  شماره 

صفحات  -

تاریخ انتشار 2014