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Tumor Necrosis Factor Receptor 2 Microsatellite and Exon 6 Polymorphisms in Rheumatoid Arthritis in Taiwan

JENG-HSIEN YEN, WEN-CHAN TSAI, CHUNG-JEN CHEN, TSAN-TENG OU, CHIA-HUI LIN, CHAUR-JONG HU, and HONG-WEN LIU

ABSTRACT.

Objective.
To investigate the role of tumor necrosis factor receptor 2 microsatellite allele (TNFR2ms) and TNFR2 exon 6 polymorphisms in the pathogenesis of rheumatoid arthritis (RA) in Taiwan.

Methods. TNFR2ms was determined in 114 patients with RA and 75 healthy controls by polymerase chain reaction (PCR) method and electrophoresis with sequencing gel. The TNFR2 exon 6 polymorphisms were also simultaneously measured by PCR restriction fragment length polymorphism method.

Results. The phenotypic and allelic frequencies of TNFR2ms 18 were significantly lower in patients with RA than in controls. The genotype frequency of TNFR2ms 16/18 was also significantly decreased in patients. In contrast, the phenotypic and allelic frequencies of TNFR2ms 15 showed a trend to be increased in patients with RA. There were no significant differences in the frequencies of various TNFR2ms and exon 6 polymorphisms concerning presence and absence of rheumatoid factor, bone erosion, rheumatoid nodules, or Sjögren's syndrome manifestation.

Conclusion. TNFR2ms 18 may have a protective effect on the development of RA in Taiwanese, while TNFR2ms 15 tends to have a precipitating effect. TNFR2 exon 6 polymorphisms are not related to susceptibility for RA. TNFR2ms and exon 6 polymorphisms were not associated with the clinical manifestations of RA in Taiwanese. A synergistic effect for susceptibility to RA was found between TNFR2ms 15 and HLA-DR4. (J Rheumatol 2003;30:438-42)

Key Indexing Terms:

TUMOR NECROSIS FACTOR RECEPTOR
MICROSATELLITE
POLYMORPHISM
RHEUMATOID ARTHRITIS


From the Division of Rheumatology, Department of Internal Medicine, Kaohsiung Medical University Hospital; Department of Internal Medicine, Kaohsiung Municipal Hsiao-Kang Hospital; Molecular Medicine Laboratory, Taipei Municipal Jen-Ai Hospital; and Department of Medicine, Kaohsiung Municipal United Hospital, Kaohsiung, Taiwan.

Supported by a grant from the National Science Council of Taiwan (NSC 88-2314-B-037-026).

J-H. Yen, MD, PhD, MSc, Professor, Kaohsiung Medical University and Kaohsiung Municipal United Hospital; W-C. Tsai, MD, PhD, Associate Professor; C-J. Chen, MD, MSc, Associate Professor; C-H. Lin, Technician; H-W. Liu, MD, Professor, Kaohsiung Medical University; T-T. Ou, MD, Attending Physician, Kaohsiung Municipal Hsiao-Kang Hospital; C-J. Hu, MD, Chief, Molecular Medicine Laboratory, Taipei Municipal Jen-Ai Hospital.

Address reprint requests to Dr. J-H. Yen, Division of Rheumatology, Department of Internal Medicine, Kaohsiung Medical University Hospital, 100 Shih-Chuan 1st Road, Kaohsiung City 807, Taiwan. E-mail: jehsye@kmu.edu.tw

Submitted August 17, 2001; revision accepted August 30, 2002.




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