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The ubiquitin ligase Peli1 negatively regulates T cell activation and prevents autoimmunity.

Chang M., Jin W., Chang J.H., Xiao Y., Brittain G.C., Yu J., Zhou X., Wang Y.H., Cheng X., Li P., Rabinovich B.A., Hwu P., Sun S.C.

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.

Nat. Immunol. 12:1002-1009(2011) [PubMed] [Europe PMC]

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