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Updated: May 28, 2026
08:37
Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
Published on: April 21, 2015
STUB1-mediated ubiquitination regulates Fli-1 stability and CD4⁺T cell activation during inflammation
Pengfei Li1, Liu Liu2, Yan Wu3
1Department of Pathology and Laboratory Medicine, Medical University of South Carolina, CRI Room 610, 173 Ashley Ave, MSC 908, Charleston, SC, 29425, USA. lippe@musc.edu.
Molecular Medicine (Cambridge, Mass.)
|May 27, 2026
Summary
The STUB1/Fli-1 pathway regulates CD4+ T cell activation in inflammatory conditions. Targeting this axis offers a new therapeutic strategy for immune-related disorders.
Area of Science:
- Immunology
- Molecular Biology
Background:
- Fli-1, an ETS transcription factor, is implicated in various inflammatory and immune disorders.
- Its role in CD4+ T cells during inflammation is not fully understood.
Purpose of the Study:
- To investigate the role and regulation of Fli-1 in CD4+ T cell responses during inflammation.
- To identify molecular mechanisms controlling Fli-1 stability and function.
Main Methods:
- Utilized CD4+ T cell-specific Fli-1 knockout mice and LPS-induced endotoxemia model.
- Assessed survival rates and splenic T cell activation.
- Investigated the STUB1/Fli-1 signaling pathway in vitro using Jurkat and HEK cells.
Main Results:
- Fli-1 is upregulated in CD4+ T cells during endotoxemia; its knockout improves survival and reduces T cell activation.
- STUB1 acts as an E3 ubiquitin ligase for Fli-1, promoting its degradation.
- Inflammatory stimuli disrupt STUB1/HSP70 interaction, stabilizing Fli-1 and enhancing T cell activation via NFκB signaling.
Conclusions:
- Identified the STUB1/Fli-1 axis as a novel regulator of CD4+ T cell function.
- This axis represents a potential therapeutic target for inflammatory diseases.
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