2011•RePub (Erasmus University Rotterdam)Open access

The Il-IL/23-17 Immune Pathway in Arthritis

Ferry Cornelissen

Open full text 0 citations

Abstract

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.

Open-access reader

About this research paper

What this paper is about

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.

Why it matters

A significance statement is not available in the OpenAlex record.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

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

Related papers

Back to paper searchBrowse research topicsOriginal source
The Il-IL/23-17 Immune Pathway in Arthritis — Research Paper | ScholarLens