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Updated: May 31, 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
RNA Helicase DDX21 Controls CD4+ T Cell Proliferation and Promotes Inflammatory Bowel Disease via Translational
Yujuan Zhang1,2,3, Chen Kan4, Xinhui Yang5
1Department of Geriatrics, Medical Center on Aging of Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Summary
The RNA helicase DDX21 (DExD-box helicase 21) drives T cell proliferation crucial for inflammatory bowel disease (IBD). Inhibiting DDX21 or ribosome biogenesis protects against IBD development.
Area of Science:
- Immunology
- Molecular Biology
- Gastroenterology
Background:
- Inflammatory bowel disease (IBD) involves aberrant T cell responses.
- The role of RNA helicases, like DDX21, in T cell pathology in IBD is not well understood.
Purpose of the Study:
- To investigate the function of DDX21 in CD4+ T cells during IBD.
- To explore DDX21's role in T cell proliferation and its potential as a therapeutic target.
Main Methods:
- Conditional deletion of Ddx21 in mouse T cells.
- Adoptive transfer colitis and DSS-induced colitis models.
- Analysis of T cell proliferation, ribosome biogenesis, and mRNA translation.
- Pharmacological inhibition of ribosome synthesis signaling with KU55933.
Main Results:
- DDX21 deletion in T cells impaired T cell homeostasis and proliferation.
- Ddx21-deficient T cells reduced colitis severity in adoptive transfer models.
- DDX21 is essential for ribosome biogenesis and TFDP1 translation post-T cell activation.
- KU55933 treatment mimicked DDX21 loss, protecting against DSS-induced colitis.
Conclusions:
- DDX21 is a critical regulator of T cell proliferation and ribosome biogenesis in the context of IBD.
- Targeting DDX21 or ribosome biogenesis pathways shows therapeutic potential for IBD and autoimmune diseases.
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