The nuclear IκB family protein IκBNS influences the susceptibility to experimental autoimmune encephalomyelitis in a murine model.

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...

Full description

Bibliographic Details
Main Authors: Shuhei Kobayashi, Akira Hara, Takayuki Isagawa, Ichiro Manabe, Kiyoshi Takeda, Takashi MaruYama
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2014-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC4210207?pdf=render
_version_ 1819264017091264512
author Shuhei Kobayashi
Akira Hara
Takayuki Isagawa
Ichiro Manabe
Kiyoshi Takeda
Takashi MaruYama
author_facet Shuhei Kobayashi
Akira Hara
Takayuki Isagawa
Ichiro Manabe
Kiyoshi Takeda
Takashi MaruYama
author_sort Shuhei Kobayashi
collection DOAJ
description 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.
first_indexed 2024-12-23T20:22:47Z
format Article
id doaj.art-815d8ac023964304b58522c64a11fb17
institution Directory Open Access Journal
issn 1932-6203
language English
last_indexed 2024-12-23T20:22:47Z
publishDate 2014-01-01
publisher Public Library of Science (PLoS)
record_format Article
series PLoS ONE
spelling doaj.art-815d8ac023964304b58522c64a11fb172022-12-21T17:32:29ZengPublic Library of Science (PLoS)PLoS ONE1932-62032014-01-01910e11083810.1371/journal.pone.0110838The nuclear IκB family protein IκBNS influences the susceptibility to experimental autoimmune encephalomyelitis in a murine model.Shuhei KobayashiAkira HaraTakayuki IsagawaIchiro ManabeKiyoshi TakedaTakashi MaruYamaThe 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.http://europepmc.org/articles/PMC4210207?pdf=render
spellingShingle Shuhei Kobayashi
Akira Hara
Takayuki Isagawa
Ichiro Manabe
Kiyoshi Takeda
Takashi MaruYama
The nuclear IκB family protein IκBNS influences the susceptibility to experimental autoimmune encephalomyelitis in a murine model.
PLoS ONE
title The nuclear IκB family protein IκBNS influences the susceptibility to experimental autoimmune encephalomyelitis in a murine model.
title_full The nuclear IκB family protein IκBNS influences the susceptibility to experimental autoimmune encephalomyelitis in a murine model.
title_fullStr The nuclear IκB family protein IκBNS influences the susceptibility to experimental autoimmune encephalomyelitis in a murine model.
title_full_unstemmed The nuclear IκB family protein IκBNS influences the susceptibility to experimental autoimmune encephalomyelitis in a murine model.
title_short The nuclear IκB family protein IκBNS influences the susceptibility to experimental autoimmune encephalomyelitis in a murine model.
title_sort nuclear iκb family protein iκbns influences the susceptibility to experimental autoimmune encephalomyelitis in a murine model
url http://europepmc.org/articles/PMC4210207?pdf=render
work_keys_str_mv AT shuheikobayashi thenuclearikbfamilyproteinikbnsinfluencesthesusceptibilitytoexperimentalautoimmuneencephalomyelitisinamurinemodel
AT akirahara thenuclearikbfamilyproteinikbnsinfluencesthesusceptibilitytoexperimentalautoimmuneencephalomyelitisinamurinemodel
AT takayukiisagawa thenuclearikbfamilyproteinikbnsinfluencesthesusceptibilitytoexperimentalautoimmuneencephalomyelitisinamurinemodel
AT ichiromanabe thenuclearikbfamilyproteinikbnsinfluencesthesusceptibilitytoexperimentalautoimmuneencephalomyelitisinamurinemodel
AT kiyoshitakeda thenuclearikbfamilyproteinikbnsinfluencesthesusceptibilitytoexperimentalautoimmuneencephalomyelitisinamurinemodel
AT takashimaruyama thenuclearikbfamilyproteinikbnsinfluencesthesusceptibilitytoexperimentalautoimmuneencephalomyelitisinamurinemodel
AT shuheikobayashi nuclearikbfamilyproteinikbnsinfluencesthesusceptibilitytoexperimentalautoimmuneencephalomyelitisinamurinemodel
AT akirahara nuclearikbfamilyproteinikbnsinfluencesthesusceptibilitytoexperimentalautoimmuneencephalomyelitisinamurinemodel
AT takayukiisagawa nuclearikbfamilyproteinikbnsinfluencesthesusceptibilitytoexperimentalautoimmuneencephalomyelitisinamurinemodel
AT ichiromanabe nuclearikbfamilyproteinikbnsinfluencesthesusceptibilitytoexperimentalautoimmuneencephalomyelitisinamurinemodel
AT kiyoshitakeda nuclearikbfamilyproteinikbnsinfluencesthesusceptibilitytoexperimentalautoimmuneencephalomyelitisinamurinemodel
AT takashimaruyama nuclearikbfamilyproteinikbnsinfluencesthesusceptibilitytoexperimentalautoimmuneencephalomyelitisinamurinemodel