AI Article Synopsis
- This study highlights the significance of TNF alpha and IL-1 beta in rheumatoid arthritis (RA) by identifying new genes influenced by these cytokines using oligonucleotide microarrays.
- Researchers utilized Affymetrix U95A GeneChips to analyze gene expression in fibroblast-like synoviocytes derived from RA patients after stimulation with TNF alpha and IL-1 beta.
- The findings revealed a range of differentially regulated genes, many of which are affected by both cytokines, suggesting shared signaling pathways, thus offering potential targets for future research in RA and other inflammatory conditions.
Article Abstract
Objective And Design: The development of therapies directed against TNF alpha and IL-1 beta has underscored the importance of these cytokines in rheumatoid arthritis (RA). In this study, oligonucleotide microarrays were used to identify novel transcriptional events mediated by TNF alpha and IL-1 beta.
Methods: In this study we have used Affymetrix U95A GeneChips representing 12,600 full-length human genes to identify transcriptional events mediated by these cytokines. Fibroblast-like synoviocytes were cultured from rheumatoid synovium from RA patients and stimulated with TNF alpha and IL-1 beta. Gene transcript levels were determined using Affymetrix U95A GeneChips representing 12,600 full-length human genes.
Results: A large number of differentially regulated genes were identified (1.7% of array-displayed genes for TNF alpha and 2.4% for IL-1 beta), and the validity of the array protocol was subsequently confirmed using real-time PCR. The majority of the differentially expressed genes were regulated by both TNF alpha and IL-1 beta, reflecting the distal signaling pathways shared by these cytokines. A large number of novel TNF alpha and IL-1 beta-regulated genes were identified.
Conclusions: A panel of novel TNF alpha- and IL-1 beta-regulated genes was identified, and these are promising candidates for further study in relation to RA and other inflammatory diseases.
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| http://dx.doi.org/10.1007/s00011-004-1315-8 | DOI Listing |
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