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CD28-inducible transcription factor DEC1 is required for efficient autoreactive CD4+ T cell response
Marc Martínez-Llordella1, Jonathan H Esensten, Samantha L Bailey-Bucktrout
1Diabetes Center, University of California, San Francisco, San Francisco, CA 94143, USA.
The Journal of Experimental Medicine
|July 24, 2013
Summary
The transcription factor DEC1 is crucial for CD4(+) T cell activation and function. Its absence impairs T cell survival, proliferation, and the development of autoimmune diseases like experimental autoimmune encephalomyelitis.
Area of Science:
- Immunology
- Molecular Biology
- Transcriptomics
Background:
- CD4(+) T cell activation involves significant gene expression changes.
- CD28 receptor co-stimulation is essential for naive T cell activation.
- The precise transcriptional effects of CD28 co-stimulation remain incompletely understood.
Purpose of the Study:
- To investigate the transcriptional consequences of CD28 co-stimulation on activated T cells.
- To elucidate the role of the transcription factor DEC1 in T cell activation and function.
Main Methods:
- Expression microarray analysis was employed to study T cell transcriptomes.
- DEC1-deficient CD4(+) T cells were analyzed for functional defects.
- Experimental autoimmune encephalomyelitis was used to assess DEC1's role in vivo.
Main Results:
- DEC1 is significantly upregulated in a CD28-dependent manner upon T cell activation.
- DEC1 deficiency leads to intrinsic defects in CD4(+) T cell survival and proliferation.
- DEC1 is critical for the production of pro-inflammatory cytokines (GM-CSF, IFN-γ, IL-2).
Conclusions:
- DEC1 acts as a key transcriptional mediator in naive CD4(+) T cell activation.
- DEC1 is essential for CD4(+) effector T cell functions and survival.
- DEC1 plays a critical role in the pathogenesis of T cell-mediated autoimmune diseases.
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