The ubiquitin ligase Peli1 negatively regulates T cell activation and prevents autoimmunity View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2011-10

AUTHORS

Mikyoung Chang, Wei Jin, Jae-Hoon Chang, Yichuan Xiao, George C Brittain, Jiayi Yu, Xiaofei Zhou, Yi-Hong Wang, Xuhong Cheng, Pingwei Li, Brian A Rabinovich, Patrick Hwu, Shao-Cong Sun

ABSTRACT

T cell activation is subject to tight regulation to avoid inappropriate responses to self antigens. Here we show that genetic deficiency in the ubiquitin ligase Peli1 caused hyperactivation of T cells and rendered T cells refractory to suppression by regulatory T cells and transforming growth factor-β (TGF-β). As a result, Peli1-deficient mice spontaneously developed autoimmunity characterized by multiorgan inflammation and autoantibody production. Peli1 deficiency resulted in the nuclear accumulation of c-Rel, a member of the NF-κB family of transcription factors with pivotal roles in T cell activation. Peli1 negatively regulated c-Rel by mediating its Lys48 (K48) ubiquitination. Our results identify Peli1 as a critical factor in the maintenance of peripheral T cell tolerance and demonstrate a previously unknown mechanism of c-Rel regulation. More... »

PAGES

1002

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ni.2090

DOI

http://dx.doi.org/10.1038/ni.2090

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1026758271

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/21874024


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