| First Author | Kobayashi S | Year | 2014 |
| Journal | PLoS One | Volume | 9 |
| Issue | 10 | Pages | e110838 |
| PubMed ID | 25347393 | Mgi Jnum | J:223097 |
| Mgi Id | MGI:5647957 | Doi | 10.1371/journal.pone.0110838 |
| Citation | Kobayashi S, et al. (2014) The nuclear IkappaB family protein IkappaBNS influences the susceptibility to experimental autoimmune encephalomyelitis in a murine model. PLoS One 9(10):e110838 |
| abstractText | The nuclear IkappaB family protein IkappaBNS is expressed in T cells and plays an important role in Interferon (IFN)-gamma and Interleukin (IL)-2 production. IkappaB-zeta, the most similar homolog of IkappaBNS, plays an important role in the generation of T helper (Th)17 cells in cooperation with RORgammat, a master regulator of Th17 cells. Thus, IkappaB-zeta deficient mice are resistant to Th17-dependent experimental autoimmune encephalomyelitis (EAE). However, IkappaB-zeta deficient mice develop the autoimmune-like Sjogren syndrome with aging. Here we found that IkappaBNS-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 RORgammat in response to Transforming Growth Factor (TGF)-beta1 and IL-6 stimulation. Thus, IkappaBNS plays a pivotal role in the generation of Th17 cells and in the control of Th17-dependent EAE. |
