期刊
NATURE IMMUNOLOGY
卷 3, 期 3, 页码 281-287出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni763
关键词
-
类别
资金
- NIDDK NIH HHS [R01DK56558] Funding Source: Medline
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK056558] Funding Source: NIH RePORTER
Itch is an E3 ubiquitin ligase that is disrupted in nonagouti-lethal or itchy mice. Itch deficiency leads to severe immune and inflammatory disorders and constant itching of the skin. Here we show that Itch(-/-) T cells show an activated phenotype and enhanced proliferation. Production of the type 2 T helper (T(H)2) cell cytokines interleukin 4 (IL-4) and IL-5 by Itch-/- T cells was augmented upon stimulation, and the T(H)2-dependent serum concentrations of immunoglobulin G1 (IgG1) and IgE in itchy mice were also increased. Molecularly, Itch associated with and induced ubiquitination of JunB, a transcription factor that is involved in T(H)2 differentiation. These results provide a molecular link between Itch deficiency and the aberrant activation of immune responses in itchy mice.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据