[Rheumatoid arthritis and interleukin-32].
Inflammatory cytokine cascade plays a pivotal role in the pathogenesis of rheumatoid arthritis. Recently, a novel human cytokine, interleukin-32, was reported to induce TNF-alpha. Interleukin-32 is expressed mainly 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 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 haematopoietic cells exacerbates collagen-induced arthritis. Herein, interleukin-32 plays an important role in the pathogenesis of rheumatoid arthritis.
Shoda
Hirofumi
H
Department of Allergy and Rheumatology, Graduate School of Medicine, the University of Tokyo.
Fujio
Keishi
K
Yamamoto
Kazuhiko
K
D000818:Animals; D001172:Arthritis, Rheumatoid / Q000503:physiopathology*; D006801:Humans; D007378:Interleukins / Q000502:physiology*; D051379:Mice
C496971:IL32 protein, human; D007378:Interleukins