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Updated: Mar 18, 2026

Adoptive Immunotherapy of iNKT Cells in Glucose-6-Phosphate Isomerase G6PI-Induced RA Mice
Published on: January 31, 2020
Immune checkpoint inhibitor-induced joint involvement
Juliette Quelain1, Julien Henry1, Rakiba Belkhir1
1Université Paris-Saclay, AP-HP, Hôpital Bicêtre, Rheumatology department, INSERM, CEA, UMR 1184, FHU CARE, IDMIT, Le Kremlin-Bicêtre, France.
Abstract:
Even though immune checkpoint inhibitors (ICI) remain effective treatments for an increasing number of cancers, they are also liable to cause immune-related adverse events (irAE). Rheumatologic manifestations occur in 5-10 % of patients. The most common rheumatologic irAEs are immune checkpoint-induced inflammatory arthritis (ICI-IA) and immune checkpoint-induced polymyalgia rheumatica (ICI-PMR). While ICI-IA can mimic rheumatoid arthritis (RA), it is predominantly immuno-negative (absence of rheumatoid factor and anti-citrullinated peptide antibodies) and can persist subsequent to r ICI cessation. ICI-PMR is usually reversible. First-line treatments consist of corticosteroids at the lowest effective doses and are given for short periods. They are aimed at reducing symptoms such as joint swelling, with minimal (if any) disruption of ICI therapy. In patients with corticoid dependence at a dose > 10 mg/day, second-line treatments include methotrexate and biologic therapy: anti-IL6 and TNF inhibitors (TNFi). Management of these manifestations requires balancing the opposed perspectives of effective arthritis control and possible cancer progression. When possible, ICI cessation should be avoided, and immunomodulating therapies are to be applied cautiously. Co-management by patients, oncologists, and rheumatologists is of crucial importance when balancing the risks and benefits of treatment.
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