The nuclear I?B family protein I?BNS influences the susceptibility to experimental autoimmune encephalomyelitis in a murine model.

ABSTRACT: The nuclear I?B family protein I?BNS is expressed in T cells and plays an important role in Interferon (IFN)-? and Interleukin (IL)-2 production. I?B-?, the most similar homolog of I?BNS, plays an important role in the generation of T helper (Th)17 cells in cooperation with ROR?t, a master regulator of Th17 cells. Thus, I?B-? deficient mice are resistant to Th17-dependent experimental autoimmune encephalomyelitis (EAE). However, I?B-? deficient mice develop the autoimmune-like Sjögren syndrome with aging. Here we found that I?BNS-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 ROR?t in response to Transforming Growth Factor (TGF)-?1 and IL-6 stimulation. Thus, I?BNS plays a pivotal role in the generation of Th17 cells and in the control of Th17-dependent EAE.

SUBMITTER: Kobayashi S 

PROVIDER: S-EPMC4210207 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature