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http://purl.uniprot.org/citations/19246939http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/19246939http://www.w3.org/2000/01/rdf-schema#comment"

Objective

Members of the tumor necrosis factor (TNF) receptor superfamily play a major role in the pathogenesis of multiple sclerosis. To elucidate the role of TNF receptors, in 53 relapsing-remitting multiple sclerosis patients, we measured the TNF receptor 1 and receptor 2 (TNF-R1 and TNF-R2) mRNA levels in peripheral blood leukocytes in natural history (n = 27) and during administration of interferon (IFN) beta-1a (n = 26).

Methods

Every 3 months for the duration of 1 year peripheral blood leukocytes were investigated by quantitative reverse transcription polymerase chain reaction. Every 6 months, MRI scans of the brain were analyzed semiquantitatively.

Results

At baseline, clinical expanded disability status scale score and TNF-R1 mRNA level were correlated. In the therapy group, the difference between T2 lesion load at baseline and after 12 months correlated negatively with the difference between TNF-R1 mRNA level at baseline and after 12 months. Subcutaneously applied IFN beta increased the amount of TNF-R1 mRNA, but partly decreased the amount of TNF-R2 mRNA in clinically and subclinically defined responders to therapy after 1 year compared to baseline.

Conclusion

This result might support the notion that due to different signal transduction properties of both receptors in the natural course of multiple sclerosis, TNF-alpha signaling in leukocytes via TNF-R1 might be beneficial, but detrimental via proinflammatory TNF-R2: part of the therapeutic efficacy of current first-line standard therapy with IFN might be due to the modulation of signal transduction pathways."xsd:string
http://purl.uniprot.org/citations/19246939http://purl.org/dc/terms/identifier"doi:10.1159/000204230"xsd:string
http://purl.uniprot.org/citations/19246939http://purl.uniprot.org/core/author"Pohle S."xsd:string
http://purl.uniprot.org/citations/19246939http://purl.uniprot.org/core/author"Hemberger J."xsd:string
http://purl.uniprot.org/citations/19246939http://purl.uniprot.org/core/author"Retzlaff K."xsd:string
http://purl.uniprot.org/citations/19246939http://purl.uniprot.org/core/author"Oschmann P."xsd:string
http://purl.uniprot.org/citations/19246939http://purl.uniprot.org/core/author"Reuss R."xsd:string
http://purl.uniprot.org/citations/19246939http://purl.uniprot.org/core/date"2009"xsd:gYear
http://purl.uniprot.org/citations/19246939http://purl.uniprot.org/core/name"Neuroimmunomodulation"xsd:string
http://purl.uniprot.org/citations/19246939http://purl.uniprot.org/core/pages"171-176"xsd:string
http://purl.uniprot.org/citations/19246939http://purl.uniprot.org/core/title"Interferon beta-1a induces tumor necrosis factor receptor 1 but decreases tumor necrosis factor receptor 2 leukocyte mRNA levels in relapsing-remitting multiple sclerosis."xsd:string
http://purl.uniprot.org/citations/19246939http://purl.uniprot.org/core/volume"16"xsd:string
http://purl.uniprot.org/citations/19246939http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/19246939
http://purl.uniprot.org/citations/19246939http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/19246939
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