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USP38 critically promotes asthmatic pathogenesis by stabilizing JunB protein.

Siyuan Chen1, Fenglin Yun1,2, Yikun Yao1

  • 1Chinese Academy of Sciences (CAS) Key Laboratory of Tissue Microenvironment and Tumor, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.

The Journal of Experimental Medicine
|September 19, 2018
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Summary
This summary is machine-generated.

The ubiquitin-specific protease USP38 is crucial for allergic asthma by stabilizing the JunB protein, a key factor in Th2 immune responses. USP38 deficiency protects mice from asthma, highlighting its role in Th2 immunity.

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Area of Science:

  • Immunology
  • Molecular Biology
  • Biochemistry

Background:

  • The T helper 2 (Th2) immune response is integral to allergic asthma development.
  • The precise molecular regulators of Th2 immunity remain incompletely understood.

Purpose of the Study:

  • To investigate the role of ubiquitin-specific protease 38 (USP38) in regulating Th2 immune responses and allergic asthma.
  • To elucidate the molecular mechanisms by which USP38 influences Th2 development and asthma pathogenesis.

Main Methods:

  • Investigated USP38 expression following T cell receptor (TCR) stimulation.
  • Assessed the impact of USP38 deficiency on Th2 cytokine production and Th2 cell differentiation in vitro and in vivo.
  • Examined the interaction between USP38 and JunB, including deubiquitination and protein stabilization.
  • Utilized mouse models of allergic asthma induced by ovalbumin (OVA) or house dust mite (HDM).

Main Results:

  • TCR stimulation up-regulated USP38 levels.
  • USP38 deficiency rendered mice resistant to OVA- or HDM-induced asthma.
  • USP38 directly interacted with JunB, deubiquitinating it and preventing its degradation.
  • USP38 was essential for TCR-induced Th2 cytokine production and Th2 cell development.

Conclusions:

  • USP38 is a critical regulator of Th2-mediated allergic asthma.
  • USP38 stabilizes JunB protein, thereby promoting Th2 development.
  • USP38 is the first identified deubiquitinase specifically involved in Th2 immunity and asthma pathogenesis.