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Updated: Aug 29, 2026

Adoptive Immunotherapy of iNKT Cells in Glucose-6-Phosphate Isomerase (G6PI)-Induced RA Mice
Published on: January 31, 2020
Rheumatoid arthritis flares and de novo inflammatory arthritis after immune checkpoint inhibitor therapy: a
Shion Kachi1, Mirei Shirakashi1, Motoo Nomura2,3
1Department of Rheumatology and Clinical Immunology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Abstract:
Immune checkpoint inhibitors (ICIs) can cause de novo inflammatory arthritis and flares of pre-existing rheumatoid arthritis (RA). This study aimed to describe and explore the clinical characteristics and treatment outcomes of these arthritis groups in a single-center, exploratory cohort. We retrospectively analyzed patients who developed inflammatory arthritis after ICI therapy, including pre-existing RA flares and the de novo cases. The de novo cases were operationally classified based on the 2010 ACR/EULAR classification criteria into those who fulfilled the criteria (ICI-RA) and those who did not (ICI-IA). Of 41 de novo cases, 10 and 31 patients were classified into ICI-RA and ICI-IA, respectively. Six patients with RA experienced flares. At baseline, serum IgA was numerically higher in the RA flare group than in the non-flare group (median 482.5 vs. 266 mg/dL). At onset, the ICI-IA group exhibited higher eosinophil counts than the RA flare group (median 140 vs. 7/µL), although prior glucocorticoid exposure may have influenced these values. At 365 days, cumulative treatment discontinuation rates were 34.1% for ICI-IA, 20.0% for ICI-RA, and 0% for RA flares. These operationally defined subgroups exhibited heterogeneous clinical courses. These hypothesis-generating findings support future prospective cohorts with detailed immunophenotyping.
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