Optineurin inhibition impedes type II collagen challenged dendritic cell migration

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. Overall design: 3 wild type and 3 OPTN knockout CII-stimulated BMDCs