Abstract
The HECT-type E3 ligase Itch is increasingly being shown to have a vital role in immune regulation. Itch deficiency leads to deleterious inflammatory disorders both in mice and humans. By adding ubiquitin to the key signaling intermediates, Itch functions as a critical regulator of lymphocyte-cell activation, differentiation and immune tolerance. Also, Itch cooperates with deubiquitinating enzymes such as A20 and Cyld to terminate NF-κB signaling and prevent chronic inflammation. This review summarizes recent advances that highlight Itch's role in lymphocyte function and explores recent insights regarding its role as a regulator of inflammatory signaling.Immunology and Cell Biology advance online publication, 13 January 2015; doi:10.1038/icb.2014.118.
Original language | English |
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Pages (from-to) | 452-460 |
Journal | Immunology and Cell Biology |
Volume | 93 |
Issue number | 5 |
DOIs | |
Publication status | Published - 2015 |
Subject classification (UKÄ)
- Immunology