Abstract
Abstract Regulatory T (Treg) cells are indispensable for the maintenance of immune tolerance and the prevention of autoimmunity; however, how Treg cells retain their homeostasis with immune suppressive function remains largely unclear. Here we report that deubiquitinase CYLD plays a critical role in the maintenance of Treg cells. Foxp3− specific CYLD knockout mice showed severe pulmonary inflammation due to preferential migration of Treg cells into the lung and increased interleukin-4 (IL-4) production compared to control mice, which was reversed by the deletion of IL-4. Genome-wide microarray analysis unveiled that Scinderin, a member of the actin-binding gelsolin family, was highly upregulated in CYLD-deficient Treg cells, which contributed to IL-4 production through complex formation with MEK/ERK. Increased IL-4 production by CYLD-deficient Treg cells was significantly rectified by Scinderin ablation. Our findings indicate that CYLD is essential to maintain Treg cell function through regulating Scinderin expression.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
