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Nat. Commun., Published: 01 July 2025 | https://doi.org/10.1038/s41467-025-60445-6
Type 1 interferon signature and allograft inflammatory factor-1 contribute to refractoriness to TNF inhibition in ankylosing spondylitis
Woogil Song1,8, Eunyoung Emily Lee2,8, Seongwan Park3,8, Baekgyu Choi3, Min-Gang Kim4, Seo Yoon Ban4, Se Rim Choi5, Jeong Yeon Kim4,6, Seon Uk Kim4, Jong-Il Kim7, Eui-Cheol Shin1, Inkyung Jung3, Jeong Seok Lee1,6, Eun Young Lee4 & the Single-Cell Atlas of Immune Diseases Consortium*
1Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon 34141, Republic of Korea.
2Division of Rheumatology, Department of Internal Medicine, Korea Cancer Center Hospital, Korea Institute of Radiological and Medical Sciences, Seoul 01812, Republic of Korea.
3Department of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon 34141, Republic of Korea.
4Division of Rheumatology, Department of Internal Medicine, Seoul National University College of Medicine, Seoul 03080, Republic of Korea.
5Hanyang University Institute for Rheumatology Research and Department of Rheumatology, Hanyang University Hospital for Rheumatic Diseases, Seoul 04763, Republic of Korea.
6Inocras, Inc, San Diego, CA 92121, USA.
7Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Republic of Korea.
8These authors contributed equally: Woogil Song, Eunyoung Emily Lee, Seongwan Park.*A list of authors and their affiliations appears at the end of the paper.
Corresponding authors
Correspondence to Inkyung Jung, Jeong Seok Lee or Eun Young Lee.
1Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon 34141, Republic of Korea.
2Division of Rheumatology, Department of Internal Medicine, Korea Cancer Center Hospital, Korea Institute of Radiological and Medical Sciences, Seoul 01812, Republic of Korea.
3Department of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon 34141, Republic of Korea.
4Division of Rheumatology, Department of Internal Medicine, Seoul National University College of Medicine, Seoul 03080, Republic of Korea.
5Hanyang University Institute for Rheumatology Research and Department of Rheumatology, Hanyang University Hospital for Rheumatic Diseases, Seoul 04763, Republic of Korea.
6Inocras, Inc, San Diego, CA 92121, USA.
7Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Republic of Korea.
8These authors contributed equally: Woogil Song, Eunyoung Emily Lee, Seongwan Park.*A list of authors and their affiliations appears at the end of the paper.
Corresponding authors
Correspondence to Inkyung Jung, Jeong Seok Lee or Eun Young Lee.
Abstract
Ankylosing spondylitis (AS) is a chronic inflammatory arthritis that primarily affects the enthesis and may culminate in bony ankylosis of the spine. Despite TNF inhibitor (TNFi) being foundational in managing active inflammation, 30-40% of patients with AS remain non-responsive. Through longitudinal and multi-omics profiling of peripheral blood mononuclear cells from TNFi-receiving patients with AS, here we reveal that elevated type I IFN signatures at baseline are associated with poor TNFi response, leading to a paradoxical enhancement of IFN signatures and Th17 responses following TNFi therapy. Among type I IFN-related genes, we identify and validate AIF-1 as a predictive biomarker reflecting the inherent IFN signature that differentiates responders from non-responders. AIF-1 also contributes to an inflammatory cycle by increasing IFNα receptor expression and Th17 responses. In summary, our findings advocate for a personalized approach to managing AS by considering individual variations in AIF-1 levels and IFN signatures.
논문정보
- Research article
- 2025년 07월 (BRIC 등록일 2025-07-02)
- 국내(교신)+국외 연구진
- 의약학 > 면역의학
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