The Il-IL/23-17 Immune Pathway in Arthritis
Ferry Cornelissen
Abstract
Open-access reader
Ferry Cornelissen
Abstract
Open-access reader
Rheumatoid arthritis (RA) was originally thought to be a T-helper (Th)1- but not a Th2- \nassociated disorder; however, it currently is unclear whether RA is a Th1- and/or Th17- \nmediated disease, and what the contributions of these T-cell subsets are in the pathogenesis \nof RA. Results from studies using different arthritis models have demonstrated that IL-17- \nproducing T-cells are the dominant cell type in the development of arthritis. In addition, a \ncritical role of the IL-23/IL-17 axis in the progression to chronic destructive arthritis has \nbeen demonstrated. Interestingly, Th1 and Th17 cells both may have unique pathogenic \npotential, and the recent insights into T-cell plasticity may change the understanding of \nthe role of T-cell subsets in chronic autoimmune diseases.
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Rheumatoid arthritis (RA) was originally thought to be a T-helper (Th)1- but not a Th2- \nassociated disorder; however, it currently is unclear whether RA is a Th1- and/or Th17- \nmediated disease, and what the contributions of these T-cell subsets are in the pathogenesis \nof RA. Results from studies using different arthritis models have demonstrated that IL-17- \nproducing T-cells are the dominant cell type in the development of arthritis. In addition, a \ncritical role of the IL-23/IL-17 axis in the progression to chronic destructive arthritis has \nbeen demonstrated. Interestingly, Th1 and Th17 cells both may have unique pathogenic \npotential, and the recent insights into T-cell plasticity may change the understanding of \nthe role of T-cell subsets in chronic autoimmune diseases.
Key concepts: Immunology, Arthritis, Interleukin 17, Pathogenesis, T cell, Immune system, Medicine, Autoimmune disease