Analysis of Fas ligand gene mutation in patients with systemic lupus erythematosus

Takeshi Kojima, Takahiko Horiuchi, Hiroaki Nishizaka, Takuya Sawabe, Masanori Higuchi, Shin Ichi Harashima, Shigeru Yoshizawa, Hiroshi Tsukamoto, Kohei Nagasawa, Yoshiyuki Niho

研究成果: Contribution to journalArticle査読

22 被引用数 (Scopus)

抄録

Objective. To investigate the possible association of a Fas ligand (FasL) gene mutation(s) or polymorphism(s) with systemic lupus erythematosus (SLE). Methods. For amplification of the introns of the FasL gene, long polymerase chain reaction (PCR) using exon-based primers was utilized, followed by partial sequencing to construct exon-specific oligonucleotide primers for the analyses of FasL genomic DNA in SLE patients. Structural defects were studied by use of a composite analysis of reverse transcriptase- PCR/single-strand conformational polymorphism (SSCP) analysis of messenger RNA (mRNA) transcripts of the FasL gene in 35 SLE patients and PCR/SSCP analysis of FasL genomic DNA in 143 SLE patients. Results. The sizes of the introns were ~0.6 kb for intron 1, 4.3 kb for intron 2, and 1.3 kb for intron 3. By SSCP analysis, we did not identify any mutations or polymorphisms in the FasL mRNA transcripts or in any of the 4 exons or areas of the introns adjacent to the exons. Conclusion. Using the same methods used in the present studies (PCR/SSCP), one group of investigators identified a structural defect of the FasL molecule in 1 of 75 SLE patients evaluated. Among the 143 SLE patients in the present study, however, we did not identify any mutations or polymorphisms of the FasL gene. Our results suggest that a FasL defect is not the major contributing factor in the pathogenesis of SLE.

本文言語英語
ページ(範囲)135-139
ページ数5
ジャーナルArthritis and rheumatism
43
1
DOI
出版ステータス出版済み - 1 2000

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Rheumatology
  • Immunology
  • Pharmacology (medical)

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