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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00004965naa a2200445 4500
001oai:DiVA.org:kth-9195
003SwePub
008081003s2006 | |||||||||||000 ||eng|
009oai:prod.swepub.kib.ki.se:1959756
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-91952 URI
0247 a https://doi.org/10.1186/ar20902 DOI
0247 a http://kipublications.ki.se/Default.aspx?queryparsed=id:19597562 URI
040 a (SwePub)kthd (SwePub)ki
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Lindberg, Johan,d 1977-u KTH,Genteknologi4 aut0 (Swepub:kth)u120i6c2
2451 0a Effect of infliximab on mRNA expression profiles in synovial tissue of rheumatoid arthritis patients
264 1b Springer Science and Business Media LLC,c 2006
338 a print2 rdacarrier
500 a QC 20100820
520 a We examined the gene expression profiles in arthroscopic biopsies retrieved from 10 rheumatoid arthritis patients before and after anti-TNF treatment with infliximab to investigate whether such profiles can be used to predict responses to the therapy, and to study effects of the therapy on the profiles. Responses to treatment were assessed using European League Against Rheumatism response criteria. Three patients were found to be good responders, five patients to be moderate responders and two patients to be nonresponders. The TNF-alpha status of the biopsies from each of the patients before treatment was also investigated immunohistochemically, and it was detected in biopsies from four of the patients, including all three of the good responders. The gene expression data demonstrate that all patients had unique gene expression signatures, with low intrapatient variability between biopsies. The data also revealed significant differences between the good responding and nonresponding patients (279 differentially expressed genes were detected, with a false discovery rate < 0.025). Among the identified genes we found that MMP-3 was significantly upregulated in good responders (log(2) fold change, 2.95) compared with nonresponders, providing further support for the potential of MMP-3 as a marker for good responses to therapy. An even more extensive list of 685 significantly differentially expressed genes was found between patients in whom TNF-alpha was found and nonresponders, indicating that TNF-alpha could be an important biomarker for successful infliximab treatment. Significant differences were also observed between biopsies taken before and after anti-TNF treatment, including 115 differentially expressed genes in the good responding group. Interestingly, the effect was even stronger in the group in which TNF-a was immunohistochemically detected before therapy. Here, 1,058 genes were differentially expressed, including many that were novel in this context (for example, CXCL3 and CXCL14). Subsequent Gene Ontology analysis revealed that several 'themes' were significantly over-represented that are known to be affected by anti-TNF treatment in inflammatory tissue; for example, immune response (GO:0006955), cell communication (GO:0007154), signal transduction (GO:0007165) and chemotaxis (GO:0006935). No genes reached statistical significance in the moderately responding or nonresponding groups. In conclusion, this pilot study suggests that further investigation is warranted on the usefulness of gene expression profiling of synovial tissue to predict and monitor the outcome of rheumatoid arthritis therapies.
650 7a TEKNIK OCH TEKNOLOGIERx Industriell bioteknik0 (SwePub)2092 hsv//swe
650 7a ENGINEERING AND TECHNOLOGYx Industrial Biotechnology0 (SwePub)2092 hsv//eng
653 a ANTITUMOR NECROSIS FACTOR; ALPHA MONOCLONAL-ANTIBODY; CELL INFILTRATE; CONCOMITANT METHOTREXATE; MICROARRAY EXPERIMENTS; BIOPSY SPECIMENS; FACTOR THERAPY; TNF-ALPHA; TRIAL; INFLAMMATION
653 a Bioengineering
653 a Bioteknik
7001 a af Klint, Eriku Department of Medicine, Karolinska Institute, Karolinska University Hospital4 aut
7001 a Catrina, Anca Irinelu Karolinska Institutet4 aut
7001 a Nilsson, Peteru KTH,Genteknologi4 aut0 (Swepub:kth)u1ws88sk
7001 a Klareskog, Larsu Karolinska Institutet4 aut
7001 a Ulfgren, Ann-Kristinu Department of Medicine, Karolinska Institute, Karolinska University Hospital4 aut
7001 a Lundeberg, Joakimu KTH,Genteknologi4 aut0 (Swepub:kth)u1qkn9kw
7102 a KTHb Genteknologi4 org
7730 t Arthritis Research & Therapyd : Springer Science and Business Media LLCg 8:6, s. R179-q 8:6<R179-x 1478-6362x 1478-6354
8564 u https://arthritis-research.biomedcentral.com/track/pdf/10.1186/ar2090
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-9195
8564 8u https://doi.org/10.1186/ar2090
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:1959756

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