Induction of the IL-1RII decoy receptor by NFAT/FOXP3 blocks IL-1β-dependent response of Th17 cellsopen access
- Authors
- Kim, Dong Hyun; Kim, Hee Young; Cho, Sunjung; Yoo, Su-Jin; Kim, Won-Ju; Yeon, Hye Ran; Choi, Kyungho; Choi, Je-Min; Kang, Seong Wook; Lee, Won-Woo
- Issue Date
- Jan-2021
- Publisher
- ELIFE SCIENCES PUBLICATIONS LTD
- Keywords
- Foxp3; IL-1 receptor; IL-1β; NFAT; Rheumatoid arthritis (RA); Th17
- Citation
- ELIFE, v.10, pp.1 - 29
- Indexed
- SCIE
SCOPUS
- Journal Title
- ELIFE
- Volume
- 10
- Start Page
- 1
- End Page
- 29
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/1651
- DOI
- 10.7554/eLife.61841
- ISSN
- 2050-084X
- Abstract
- 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.
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