Review Article

J Rheum Dis 2017; 24(1): 14-20

Published online February 28, 2017

© Korean College of Rheumatology

Interleukin-32 Gamma as a New Face in Inflammatory Bone Diseases

Eun-Jin Lee*, Bongkun Choi*, Eui-Seung Hwang, Eun-Ju Chang

Department of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea

Correspondence to : Eun-Ju Chang, Department of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, 88 Olympic-ro 43-gil, Songpa-gu, Seoul 05505, Korea. E-mail : ejchang@amc.seoul.kr

Received: February 13, 2017; Revised: February 14, 2017; Accepted: February 14, 2017

This is a Open Access article, which permits unrestricted non-commerical use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Interleukin-32 (IL-32), a recently identified pro-inflammatory cytokine, is involved in the pathogenesis and progression of infections, cancer, chronic inflammation, and autoimmune disease. IL-32γ is the most active isoform in cell death and cell activation among nine distinct isoforms of IL-32. IL-32γ potentiates both osteogenic and osteoclastogenic capacities, and is critical in the coupling of bone resorption and bone formation for maintenance of bone homeostasis. IL-32γ is strongly associated with inflammatory bone disorders such as rheumatoid arthritis, ankylosing spondylitis, and osteoporosis. In this review, we summarize current research on the role of IL-32γ in inflammatory bone disorders, highlighting this cytokine as a novel target for prognostic marker and control of these diseases.

Keywords IL-32γ, Osteogenesis, Rheumatoid arthritis, Ankylosing spondylitis, Osteoporosis

Article

Review Article

J Rheum Dis 2017; 24(1): 14-20

Published online February 28, 2017 https://doi.org/10.4078/jrd.2017.24.1.14

Copyright © Korean College of Rheumatology.

Interleukin-32 Gamma as a New Face in Inflammatory Bone Diseases

Eun-Jin Lee*, Bongkun Choi*, Eui-Seung Hwang, Eun-Ju Chang

Department of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea

Correspondence to:Eun-Ju Chang, Department of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, 88 Olympic-ro 43-gil, Songpa-gu, Seoul 05505, Korea. E-mail : ejchang@amc.seoul.kr

Received: February 13, 2017; Revised: February 14, 2017; Accepted: February 14, 2017

This is a Open Access article, which permits unrestricted non-commerical use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Interleukin-32 (IL-32), a recently identified pro-inflammatory cytokine, is involved in the pathogenesis and progression of infections, cancer, chronic inflammation, and autoimmune disease. IL-32γ is the most active isoform in cell death and cell activation among nine distinct isoforms of IL-32. IL-32γ potentiates both osteogenic and osteoclastogenic capacities, and is critical in the coupling of bone resorption and bone formation for maintenance of bone homeostasis. IL-32γ is strongly associated with inflammatory bone disorders such as rheumatoid arthritis, ankylosing spondylitis, and osteoporosis. In this review, we summarize current research on the role of IL-32γ in inflammatory bone disorders, highlighting this cytokine as a novel target for prognostic marker and control of these diseases.

Keywords: IL-32γ, Osteogenesis, Rheumatoid arthritis, Ankylosing spondylitis, Osteoporosis

JRD
Oct 01, 2024 Vol.31 No.4, pp. 191~263
COVER PICTURE
Ancestry-driven pathways for SLE-risk SNP-associated genes. The ancestry-driven key signaling pathways in Asians, Europeans, and African Americans were analyzed by enrichr (https://maayanlab.cloud/Enrichr/#libraries) using non-HLA SNP-associated genes. SLE: systemic lupus erythematosus, SNP: single-nucleotide polymorphism, JAK–STAT: janus kinase–signal transducers and activators of transcription, IFN: interferon gamma. (J Rheum Dis 2024;31:200-211)

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