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Optineurin inhibition impedes type II collagen challenged dendritic cell migration

GSE240706 Mus musculus Expression profiling by high throughput sequencing 6 samples Submitted 2025/05/22 Platform GPL13112
Summary
Due to the maturation, migration and antigen presentation functions, dendritic cells (DCs) play a central role in the development of many autoimmune diseases, like rheumatoid arthritis, multiple sclerosis and dermatitis. However, the molecular regulatory process of disease- or antigen-specific DC activation remains elusive. We show that deletion of Optineurin (OPTN) effectively impairs type II collagen (CII), the main autoantigen for rheumatoid arthritis, challenged DC migration, thus ameliorating collagen-induced arthritis. Transcriptome analyses indicate that OPTN promotes the expressions of migration related genes. Our findings thus indicate that OPTN is an important regulator of CII-pulsed DC migration, which may be of potential value for the accurate treatment of rheumatoid arthritis.
Published in
Optineurin restrains CCR7 degradation to guide type II collagen-stimulated dendritic cell migration in rheumatoid arthritis
Hong W, Ma H, Yang Z et al. · Acta pharmaceutica Sinica. B 2025 · PMID 40370566 · doi:10.1016/j.apsb.2025.02.004
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Also filed as BioProject PRJNA1004646 and SRA study SRP454695. Searching any of these in the dataset finder brings you back here.

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