Ubc13 maintains the suppressive function of regulatory T cells and prevents their conversion into effector-like T cells

Title
Ubc13 maintains the suppressive function of regulatory T cells and prevents their conversion into effector-like T cells
Author(s)
장재훈Yichuan Xiao[Yichuan Xiao]Hongbo Hu[Hongbo Hu]Jin Jin[Jin Jin]Jiayi Yu[Jiayi Yu]Xiaofei Zhou[ Xiaofei Zhou]Xuefeng Wu[Xuefeng Wu]Howard M Johnson[Howard M Johnson]Shizuo Akira[Shizuo Akira]Manolis Pasparakis[Manolis Pasparakis]Shao-Cong Sun[Shao-Cong Sun]Xuhong Cheng[Xuhong Cheng]
Keywords
TRANSCRIPTION FACTOR; UBIQUITIN LIGASE; CUTTING EDGE; TH17 CELLS; IFN-GAMMA; IN-VIVO; FOXP3; ACTIVATION; EXPRESSION; INHIBITION
Issue Date
201205
Publisher
NATURE PUBLISHING GROUP
Citation
NATURE IMMUNOLOGY, v.13, no.5, pp.481 - U84
Abstract
The maintenance of immune homeostasis requires regulatory T cells (T-reg cells). Here we found that T-reg cell-specific ablation of Ubc13, a Lys63 (K63)-specific ubiquitin-conjugating enzyme, caused aberrant T cell activation and autoimmunity. Although Ubc13 deficiency did not affect the survival of T-reg cells or expression of the transcription factor Foxp3, it impaired the in vivo suppressive function of T-reg cells and rendered them sensitive to the acquisition of T helper type 1 (T(H)1) cell-and interleukin 17 (IL-17)-producing helper T (T(H)17) cell-like effector phenotypes. This function of Ubc13 involved its downstream target, the kinase IKK. The Ubc13-IKK signaling axis controlled the expression of specific T-reg cell effector molecules, including IL-10 and SOCS1. Collectively, our findings suggest that the Ubc13-IKK signaling axis regulates the molecular program that maintains T-reg cell function and prevents T-reg cells from acquiring inflammatory phenotypes.
URI
http://hdl.handle.net/YU.REPOSITORY/28260http://dx.doi.org/10.1038/ni.2267
ISSN
1529-2908
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약학대학 > 약학부 > Articles
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