期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 215, 期 11, 页码 2850-2867出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20172026
关键词
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资金
- National Natural Science Foundation of China [81430036, 91542119, 91429307]
- National Key Research and Development Program of China [2018YFA0507402]
- Strategic Priority Research Program of the Chinese Academy of Sciences [XDB19000000]
Th2 immune response is critical for allergic asthma pathogenesis. Molecular mechanisms for regulating Th2 immunity are still not well understood. Here we report that the ubiquitin-specific protease USP38 is crucial for Th2-mediated allergic asthma. TCR stimulation up-regulated the USP38 level, and USP38 in turn mediated the protein stabilization of JunB, a transcription factor specific for Th2 development. Consequently, USP38 was specifically required for TCR-induced production of Th2 cytokines and Th2 development both in vitro and in vivo, and USP38-deficient mice were resistant to asthma pathogenesis induced by OVA or HDM. Mechanistically, USP38 directly associated with JunB, deubiquitinated Lys-48-linked poly-ubiquitination of JunB, and consequently blocked TCR-induced JunB turnover. USP38 represents the first identified deubiquitinase specifically for Th2 immunity and the associated asthma.
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