Rheumatoid arthritis and interleukin-32.

Abstract

The inflammatory cytokine cascade plays a pivotal role in the pathogenesis of rheumatoid arthritis. Recently, a novel human cytokine, interleukin-32, was reported to induce tumor necrosis factor (TNF)-alpha. Interleukin-32 is expressed primarily in lymphoid tissues and leukocytes, but also in stimulated epithelial cells and synovial fibroblasts. Although the interleukin-32 receptor has not been reported, interleukin-32 can induce other inflammatory cytokines such as TNF-alpha, interleukin-1beta, and interleukin-6 from monocytes/macrophages in vitro and in vivo, and it synergizes with signals from pattern-recognition receptors. Notably, in the inflamed synovial tissues from rheumatoid arthritis patients, interleukin-32 is prominently expressed and correlates with the severity of arthritis and the expression of other cytokines, including TNF-alpha and interleukin-1. In experimental mice models of arthritis, joint injection of interleukin-32 induces joint inflammation, and overexpression of interleukin-32beta in hematopoietic cells exacerbates collagen-induced arthritis. Interleukin-32 can thus be seen to play an important role in the pathogenesis of rheumatoid arthritis.

• Authors: H Shoda, K Fujio, K Yamamoto
• Journal: Cellular and molecular life sciences : CMLS (Cell Mol Life Sci) Vol. 64 Issue 19-20 Pg. 2671-9 (Oct 2007) ISSN: 1420-682X [Print] Switzerland
• PMID: 17619821 (Publication Type: Journal Article, Review)

Chemical References

• Cytokines
• IL32 protein, human
• Interleukins

Topics

• Animals
• Arthritis, Rheumatoid (etiology)
• Cytokines (genetics)
• Gene Expression Regulation
• Humans
• Inflammation
• Interleukins (genetics, physiology)
• Mice