Immune Netw.  2007 Mar;7(1):10-17. 10.4110/in.2007.7.1.10.

The Th17 and Autoimmune Arthritis

• Cho ML
• Heo YJ
• Park JS
• Lee SY
• Sung YC
• Kim HY

• KMID: 2150622
• DOI: http://doi.org/10.4110/in.2007.7.1.10

Abstract

Autoimmune arthritis, such as rheumatoid arthritis (RA), is a chronic inflammatory disorder that primarily affects the joints and then results in their progressive destruction. Effector Th cells have been classified as Th1 and Th2 subsets based on their cytokine expression profiles and immune regulatory function. Another subset of T cells termed Th17 was recently discovered and known to selectively produce IL-17. Also, Th17 was shown to be generated by TGFbeta and IL-6 and maintained by IL-23. IL-17 is a proinflammatory cytokine that is considered to involve the development of various inflammatory autoimmune diseases such as RA, asthma, lupus, and allograft rejection. IL-17 is present in the sera, synovial fluids and synovial biopsies of most RA patient. IL-17 activates RA synovial fibroblasts to synthesize IL-6, IL-8 and VEGF via PI3K/Akt and NF-kappaB dependent pathway. IL-17 increases IL-6 production, collagen destruction and collagen synthesis. In addition, it not only causes bone resorption but also increases osteoclastogenesis and fetal cartilage destruction. Inhibition of the IL-17 production may contribute a novel therapeutic approach along with potent anti-inflammatory effect and with less immunosuppressive effect on host defenses.

Keyword

Autoimmune arthritis; IL-17; Th17

MeSH Terms

Allografts
Arthritis*
Arthritis, Rheumatoid
Asthma
Autoimmune Diseases
Biopsy
Bone Resorption
Cartilage
Collagen
Fibroblasts
Humans
Interleukin-17
Interleukin-23
Interleukin-6
Interleukin-8
Joints
NF-kappa B
Synovial Fluid
T-Lymphocytes
Transforming Growth Factor beta
Vascular Endothelial Growth Factor A
Collagen
Interleukin-17
Interleukin-23
Interleukin-6
Interleukin-8
NF-kappa B
Transforming Growth Factor beta
Vascular Endothelial Growth Factor A