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TNF-α blockade induces IL-10 expression in human CD4+ T cells
Hayley G Evans1, Urmas Roostalu1, Gina J Walter1
1Centre for Molecular & Cellular Biology of Inflammation (CMCBI), Division of Immunology, Infection and Inflammatory Disease, King's College London, SE1 1UL, UK.
Nature Communications
|February 5, 2014
Summary
Tumor necrosis factor inhibitors (TNFi) increase the anti-inflammatory cytokine IL-10 in CD4+ T cells, including those driving inflammation. This TNFi-induced IL-10 production in Th17 cells involves the transcription factor Aiolos.
Area of Science:
- Immunology
- Molecular Biology
- Inflammation Research
Background:
- Interleukin-17-producing CD4+ T (Th17) cells are key players in inflammatory diseases.
- Understanding how therapies modulate these cells is crucial for disease management.
Purpose of the Study:
- To investigate the effect of TNF inhibitors (TNFi) on CD4+ T cells, particularly Th17 cells.
- To elucidate the molecular mechanisms underlying TNFi-induced changes in these cells.
Main Methods:
- Flow cytometry and gene expression analysis of CD4+ T cells from patients treated with TNFi.
- Investigation of the role of Interleukin-10 (IL-10) and the transcription factor IKZF3 (Aiolos).
Main Results:
- TNFi drugs induce the anti-inflammatory cytokine IL-10 in CD4+ T cells, including Th17 cells.
- This induction is independent of regulatory T cells (Treg) and Foxp3, requires IL-10, and can be reversed by IL-1β.
- TNFi-treated Th17 cells show a distinct gene signature including IL10 and IKZF3, with Aiolos binding to the IL10 locus.
- Aiolos overexpression drives IL-10 production in CD4+ T cells.
Conclusions:
- TNF-α blockade by TNFi induces IL-10 production in CD4+ T cells, including Th17 cells.
- The transcription factor Aiolos plays a significant role in regulating IL-10 expression within CD4+ T cells.
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