DNA Research Advance Access originally published online on February 23, 2006
DNA Research 2005 12(6):429-439; doi:10.1093/dnares/dsi020
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Isolation and Expression Profiling of Genes Upregulated in the Peripheral Blood Cells of Systemic Lupus Erythematosus Patients
1Department of Molecular Medicine, Graduate School of Medicine, Osaka University Suita, Japan
2Department of Hematology and Oncology, Graduate School of Medicine, Osaka University Suita, Japan
3Division of Allergy, Osaka Prefectural Medical Center for Respiratory and Allergic Diseases Habikino, Japan
4Innovation Plaza Osaka Izumi, Japan
5Department of Molecular Genetics, Research Institute for Microbial Diseases, Osaka University Suita, Japan
6Department of Rheumatology Kawachinagano, Japan
7Department of Allergology Kawachinagano, Japan
8Department of Clinical Research Kawachinagano, Japan
9NHO Osaka-Minami Medical Center Kawachinagano, Japan
10Department for Immunologic Diseases, Kinki-Central Hospital Itami, Japan
11Department of Internal Medicine, Nissay Hospital Osaka, Japan
12Department of Rheumatology, Osaka General Medical Center Osaka, Japan
We have identified the genes whose expressions are augmented in the blood cells of the patients with systemic lupus erythematosus (SLE) using the stepwise subtraction technique along with microarray analysis. The expression levels of these genes were assessed by quantitative real-time reverse transcription polymerase chain reaction (RTPCR) in 31 SLE patients and 30 healthy controls. We found that the transcription levels of following eight genes were significantly increased in SLE patients; interferon (IFN)-
-inducible protein 27 (IFI27), IFN-
-inducible protein IFI-15K (G1P2), IFN stimulated gene 20 kDa (ISG20), epithelial stromal interaction 1 (EPSTI1), defensin-
(DEFA3), amphiregulin (AREG) and two genes of unknown function (BLAST accession nos AL050290 and AY358224 = SLED1). In comparison with idiopathic thrombocytopenic purpura (ITP), an organ-specific autoimmune disease, IFI27, G1P2 and SLED1 were preferentially upregulated in SLE. In contrast, AREG and AL050290 were more highly expressed in ITP than in SLE. We correlated changes in gene expression and clinical/laboratory features of SLE and found that expression of ISG20, EPSTI1 and SLED1 are significantly correlated with lymphocyte counts. Genes linked to IFN are well known to influence SLE, but several other novel genes unrelated to IFN signaling we report here would be useful to understand the pathophysiology of SLE.
Key words: stepwise subtraction; microarray; SLE; ITP; interferon; G0S2; amphiregulin
*To whom correspondence should be addressed. Tel. +81-6-6875-3980, Fax. +81-6-6875-5192, E-mail: snj-0212{at}biken.osaka-u.ac.jp
Communicated by Mitsuo Oshimura
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