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Review : Decreased tumour necrosis factor-beta production in TNFB*2 homozygote: an important predisposing factor of lupus nephritis in Koreans

Department of Internal Medicine, Lupus Clinic of Rheumatism Centre, Kangnam St Mary's Hospital

Sung-Hwan Park

Department of Internal Medicine, Lupus Clinic of Rheumatism Centre, Kangnam St Mary's Hospital

Jun-Ki Min

Department of Internal Medicine, Lupus Clinic of Rheumatism Centre, Kangnam St Mary's Hospital

Sung-Il Kim

Department of Internal Medicine, Lupus Clinic of Rheumatism Centre, Kangnam St Mary's Hospital

Wan-Hee Yoo

Department of Internal Medicine, Lupus Clinic of Rheumatism Centre, Kangnam St Mary's Hospital

Yeon-Sik Hong

Department of Internal Medicine, Lupus Clinic of Rheumatism Centre, Kangnam St Mary's Hospital

Jae-Ho Park

Department of Internal Medicine, Lupus Clinic of Rheumatism Centre, Kangnam St Mary's Hospital

Chul-Soo Cho

Department of Internal Medicine, Lupus Clinic of Rheumatism Centre, Kangnam St Mary's Hospital

Tai-Gyu Kim

Department of Microbiology, College of Medicine, the Catholic University of Korea, Seoul, Korea

Hoon Han

Department of Microbiology, College of Medicine, the Catholic University of Korea, Seoul, Korea

Ho-Youn Kim

Department of Internal Medicine, Lupus Clinic of Rheumatism Centre, Kangnam St Mary's Hospital

Low TNF production and its association with TNF gene restriction fragment length polymorphism (RFLP) was demonstrated in (NZW/NZB) F₁ mice. However, little is known about the significance of TNF production in association with TNF gene polymorphism in human SLE. This study was designed to evaluate the role of TNF production of peripheral blood mononuclear cells (PBMC) and its association with TNFB gene polymorphism in SLE, particularly lupus nephritis. TNFB gene polymorphism was defined by PCR-NcoI RFLP. TNF productions of phytohemagglutinin (PHA)- stimulated PBMC and T cells were examined by bioassay using L929 cell line and ELISA. The PBMC stimulated by PHA from patients with SLE (n = 60) tended to secrete less amounts of TNF by bioassay (1032±184pg/ml vs 1524±224pg/ml, P=0.094), and TNF-ß by ELISA (P = 0.0082) than that from normal controls (n = 38). The low TNF- producer was more frequent in nephritis than non-nephritis (34.4% vs 7.1% respectively, P<0.01). TNF-ß also revealed similar results (53.1% vs 21.4%, P<0.05). In SLE, mean production of TNF-ß was decreased in TNFB*2 homozygote ( n=18) than that in TNFB*1 homozygote (n = 9) (1126.3±145 pg/ml) vs 642 ± 118.4 pg/ml, respectively, P = 0.021), whereas TNF- production showed little difference between the two groups (710.1 ± 56.4 vs 542.4 ± 71.1 pg/ml, respectively, P = 0.149). Our results demonstrate that decreased TNF production of PBMC, which was significantly associated with TNFB*2 homozygosity, could be an important predisposing factor of lupus nephritis in Koreans.

Key Words: SLE • TNFB gene • TNF-beta • lupus nephritis

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