Rheumatology 2002; 41: 518-524
© 2002 British Society for Rheumatology
Original Papers |
Genetically determined interferon-
production influences the histological phenotype of lupus nephritis
Department of Medicine and Biosystemic Science and
1 Department of Medicine and Clinical Science, Graduate School of Medical Science, Kyushu University, Fukuoka, Japan
Objective. To clarify whether the interferon-
(IFN-) gene (IFNG) is associated with the histological phenotype of lupus nephritis.
Method. We analysed microsatellite polymorphisms located within the first intron of the IFNG gene to determine the genotypes of patients with lupus nephritis WHO class IV (n=24), patients with WHO class V (n=12) and healthy controls (n=61). We used flow cytometric detection of intracellular cytokines to identify CD4+ T cells producing IFN-. Production of IFN- by peripheral blood mononuclear cells after stimulation with phytohaemagglutinin was evaluated with an enzyme-linked immunosorbent assay.
Result. The frequency of the IFNG allele 114 was significantly greater in WHO class V patients than in WHO class IV patients. Furthermore, the IFNG 114 +/+ genotype was more frequent in WHO class V than in WHO class IV patients. The level of IFN- and the percentage of IFN--producing CD4+ T cells were lower in individuals with genotype 114 +/+ than in individuals with genotype 114 -/-.
Conclusion. The IFN- gene is associated with the histological phenotype in lupus nephritis.
KEY WORDS: Lupus nephritis, WHO IV and V, Interferon-, Th1/Th2 balance, Microsatellite polymorphism.
Correspondence to: H. Nakashima, Department of Medicine and Biosystemic Science, Graduate School of Medical Science, Kyushu University, Fukuoka, Japan, Maidashi 3-1-1 Higashi-ku, Fukuoka, 812-8582, Japan.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  M. Harigai, M. Kawamoto, M. Hara, T. Kubota, N. Kamatani, and N. Miyasaka Excessive Production of IFN-{gamma} in Patients with Systemic Lupus Erythematosus and Its Contribution to Induction of B Lymphocyte Stimulator/B Cell-Activating Factor/TNF Ligand Superfamily-13B J. Immunol., August 1, 2008; 181(3): 2211 - 2219. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 O. H. Kantarci, D. D. Hebrink, J. Schaefer-Klein, Y. Sun, S. Achenbach, E. J. Atkinson, S. Heggarty, A. C. Cotleur, M. de Andrade, K. Vandenbroeck, et al. Interferon Gamma Allelic Variants: Sex-Biased Multiple Sclerosis Susceptibility and Gene Expression Arch Neurol, March 1, 2008; 65(3): 349 - 357. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Chinoy, F. Salway, S. John, N. Fertig, B. D Tait, C. V Oddis, W. E R Ollier, R. G Cooper, and The UK Adult Onset Myositis Immunogenetic Collabor Interferon-gamma and interleukin-4 gene polymorphisms in Caucasian idiopathic inflammatory myopathy patients in UK Ann Rheum Dis, July 1, 2007; 66(7): 970 - 973. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Kitawaki, H. Koshiba, Y. Kitaoka, M. Teramoto, G. Hasegawa, N. Nakamura, T. Yoshikawa, M. Ohta, H. Obayashi, and H. Honjo Interferon-{gamma} gene dinucleotide (CA) repeat and interleukin-4 promoter region (-590C/T) polymorphisms in Japanese patients with endometriosis Hum. Reprod., August 1, 2004; 19(8): 1765 - 1769. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Fransen, G. Stucki, and P. van Riel The merits of monitoring: should we follow all our rheumatoid arthritis patients in daily practice? Rheumatology, June 1, 2002; 41(6): 601 - 604. [Full Text] [PDF]
|
|