Published in Volume 123, Issue 11 (November 1, 2013)
J Clin Invest. 2013;123(11):4576–4578. doi:10.1172/JCI72477.
Copyright © 2013, American Society for Clinical Investigation
J Clin Invest. 2013;123(11):4576–4578. doi:10.1172/JCI72477.
Copyright © 2013, American Society for Clinical Investigation
Commentary
Mucosal Immunology Section, OPCB, NIDCR, NIH, Bethesda, Maryland, USA.
Address correspondence to: WanJun Chen, Mucosal Immunology Section, NIDCR, NIH, 30 Convent Dr., Bethesda, Maryland 20892, USA. Phone: 301.435.7168; Fax: 301.402.1064; E-mail: wchen@dir.nidcr.nih.gov.
First published October 25, 2013
Regulatory T cells (Tregs) control type 2 T helper cell–mediated (Th2-mediated) lung inflammation, but the molecular mechanisms by which Tregs execute this activity remain elusive. In this issue of the JCI, Jin et al. reveal that Itch, a HECT-type E3 ubiquitin ligase in Tregs, plays a specific role in restraining Th2 cell responses. This finding has important implications for understanding the pathogenesis of allergy and asthma.
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