Induction of the IL-1RII decoy receptor by NFAT/FoxP3 blocks IL-1β-dependent response of TH17 cells

Dong Hyun Kim, Hee Young Kim, Sunjung Cho, Su Jin Yoo, Won Ju Kim, Hye Ran Yeon, Kyungho Choi, Je Min Choi, Seong Wook Kang, Won Woo Lee

Research output: Contribution to journalArticlepeer-review

6 Scopus citations


Derived from a common precursor cell, the balance between Th17 and Treg cells must be maintained within immune system to prevent autoimmune diseases. IL-1β-mediated IL-1 receptor (IL-1R) signaling is essential for Th17-cell biology. Fine-tuning of IL-1R signaling is controlled by two receptors, IL-1RI and IL-RII, IL-1R accessory protein, and IL-1R antagonist. We demonstrate that the decoy receptor, IL-1RII, is important for regulating IL-17 responses in TCR-stimulated CD4+ T cells expressing functional IL-1RI via limiting IL-1β responsiveness. IL-1RII expression is regulated by NFAT via its interaction with Foxp3. The NFAT/FOXP3 complex binds to the IL-1RII promoter and is critical for its transcription. Additionally, IL-1RII expression is dysregulated in CD4+ T cells from patients with rheumatoid arthritis. Thus, differential expression of IL-1Rs on activated CD4+ T cells defines unique immunological features and a novel molecular mechanism underlies IL-1RII expression. These findings shed light on the modulatory effects of IL-1RII on Th17 responses.

Original languageEnglish
Article numbere61841
Pages (from-to)1-72
Number of pages72
StatePublished - Jan 2021


  • Foxp3
  • IL-1 receptor
  • IL-1β
  • NFAT
  • Rheumatoid arthritis (RA)
  • Th17


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