Original

The Journal of the Korean Rheumatism Association 2005; 12(2): 108-115

Published online June 30, 2005

© Korean College of Rheumatology

류마티스 관절염에서 염증 관여 유전자의 다형성 연구: 대식 세포 유주 억제 인자(MIF)

송주경·신현영·이유선·황재희·권양숙*·정연주*·이윤종**·강성욱

충남대학교 의과대학 내과학교실, 서울특별시립동부병원 방사선과*, 서울대학교 의과대학 내과학교실**

Association between Macrophage Migration Inhibitory Factor Gene Polymorphism and Rheumatoid Arthritis

Ju Kyoung Song, M.D., Hyun Young Shin, M.D., You Sun Lee, M.D., Jae Hee Hwang, M.D., Yang Sook Kwon, M.D.*, Yeon Ju Jeong, M.D.*, Yun Jong Lee, M.D.**, Seong Wook Kang, M.D.

Department of Internal Medicine, Chungnam National University College of Medicine, Daejeon, Department of Radiology, Seoul Municipal Dong-bu Hospital*, Seoul, Department of Internal Medicine, Seoul National University Bundang Hospital**, Seongnam, Korea

Correspondence to : Seong Wook Kang

Abstract

Objective: Rheumatoid arthritis (RA) is characterized by the interaction of multiple mediators, especially cytokines. Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine and has been shown to be involved in RA. This study explored the association of the MIF gene polymorphism with RA in Korean. Methods: 114 patients with RA, and 114 age and gender matched healthy controls were studied. Patients and controls were genotyped for a single nucleotide polymorphism (SNP) in the 5'-flanking region at position ⁣173 of the MIF gene. Results: No significant differences in MIF gene polymorphism were observed in RA compared to healthy controls. No association with disease severity was detected for the MIF gene polymorphism. Conclusion: MIF ⁣173 G/C polymorphism did not appear to be associated with genetic susceptibility and disease severity in Korean RA patients.

Keywords Rheumatoid arthritis, Macrophage migration inhibitory factor, Polymorphism

Article

Original

The Journal of the Korean Rheumatism Association 2005; 12(2): 108-115

Published online June 30, 2005

Copyright © Korean College of Rheumatology.

류마티스 관절염에서 염증 관여 유전자의 다형성 연구: 대식 세포 유주 억제 인자(MIF)

송주경·신현영·이유선·황재희·권양숙*·정연주*·이윤종**·강성욱

충남대학교 의과대학 내과학교실, 서울특별시립동부병원 방사선과*, 서울대학교 의과대학 내과학교실**

Association between Macrophage Migration Inhibitory Factor Gene Polymorphism and Rheumatoid Arthritis

Ju Kyoung Song, M.D., Hyun Young Shin, M.D., You Sun Lee, M.D., Jae Hee Hwang, M.D., Yang Sook Kwon, M.D.*, Yeon Ju Jeong, M.D.*, Yun Jong Lee, M.D.**, Seong Wook Kang, M.D.

Department of Internal Medicine, Chungnam National University College of Medicine, Daejeon, Department of Radiology, Seoul Municipal Dong-bu Hospital*, Seoul, Department of Internal Medicine, Seoul National University Bundang Hospital**, Seongnam, Korea

Correspondence to:Seong Wook Kang

Abstract

Objective: Rheumatoid arthritis (RA) is characterized by the interaction of multiple mediators, especially cytokines. Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine and has been shown to be involved in RA. This study explored the association of the MIF gene polymorphism with RA in Korean. Methods: 114 patients with RA, and 114 age and gender matched healthy controls were studied. Patients and controls were genotyped for a single nucleotide polymorphism (SNP) in the 5'-flanking region at position ⁣173 of the MIF gene. Results: No significant differences in MIF gene polymorphism were observed in RA compared to healthy controls. No association with disease severity was detected for the MIF gene polymorphism. Conclusion: MIF ⁣173 G/C polymorphism did not appear to be associated with genetic susceptibility and disease severity in Korean RA patients.

Keywords: Rheumatoid arthritis, Macrophage migration inhibitory factor, Polymorphism

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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