AI Article Synopsis
- FOXP3 is essential for the development and function of regulatory T cells (Tregs), but its regulation under inflammatory conditions is not well understood.
- The study found that the combination of TGF-β and IL-6 can significantly reduce FOXP3 levels by triggering its degradation, despite not affecting the stability of FOXP3 mRNA.
- The use of a proteasome inhibitor (MG132) showed promise in preventing the degradation of FOXP3, suggesting a potential method for enhancing Treg activity during inflammation.
Article Abstract
The forkhead family transcription factor FOXP3 is critical for the differentiation and function of CD4(+) CD25(+) regulatory T cells (Treg). How FOXP3 protein level is negatively regulated under the inflammatory microenvironment is largely unknown. Here we report that the combination of transforming growth factor-beta (TGF-β) and IL-6 treatment (IL-6/TGF-β) can synergistically downregulate FOXP3 at the posttranslational level by promoting FOXP3 protein degradation. In our FOXP3 overexpression model, we found that IL-6/TGF-β treatment upregulated IL-6R expression but did not affect the stability of FOXP3 mRNA. Moreover, we found that the proteasome inhibitor MG132 could inhibit IL-6/TGF-β-mediated downregulation of FOXP3 protein, which reveals a potential pathway for modulating Treg activity by preventing FOXP3 degradation during inflammation.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3438759 | PMC |
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