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A High Resolution Method to Monitor Phosphorylation-dependent Activation of IRF3
Published on: January 24, 2016
Interferon regulatory factor 3 controls interleukin-17 expression in CD8 T lymphocytes.
Laure Ysebrant de Lendonck1, Sandrine Tonon, Muriel Nguyen
1Institute for Medical Immunology, Walloon Excellence in Life sciences and BIOtechnology, Université Libre de Bruxelles, B-6041 Charleroi-Gosselies, Belgium.
Summary
Interferon regulatory factor 3 (IRF3) unexpectedly controls CD8 T-cell polarization by repressing IL-17. IRF3 directly inhibits the transcription factor RORγt, impacting T-cell activation and cytokine production.
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- Interferon regulatory factor (IRF) 3 is crucial for innate antiviral immunity.
- Its role in adaptive immune responses, particularly T-cell activation, remains less understood.
Purpose of the Study:
- To investigate the function of IRF3 in CD8 T-cell activation and polarization.
- To elucidate the molecular mechanisms by which IRF3 influences T-cell responses.
Main Methods:
- Analysis of IL-17 and IL-23R expression in wild-type and IRF3-deficient CD8 T cells.
- Adoptive transfer experiments using IRF3-deficient OT1 cells.
- Assessment of IRF3 interaction with RORγt and its effect on IL-17 promoter activity.
Main Results:
- IRF3 activation in CD8 T cells represses IL-17 production independently of type I interferon.
- IRF3-deficient CD8 T cells exhibit enhanced IL-17 and IL-23R expression.
- IRF3 directly binds to RORγt, inhibiting its transactivation of the IL-17 promoter.
Conclusions:
- IRF3 plays a novel inhibitory role in CD8 T-cell polarization towards IL-17-producing cells.
- IRF3 acts intrinsically within T cells to regulate RORγt activity and IL-17 expression.
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