Comparison of IFN-β inducible gene expression in primary-progressive and relapsing-remitting multiple sclerosis
Journal of Neuroimmunology, ISSN: 0165-5728, Vol: 265, Issue: 1, Page: 68-74
2013
- 5Citations
- 30Captures
Metric Options: CountsSelecting the 1-year or 3-year option will change the metrics count to percentiles, illustrating how an article or review compares to other articles or reviews within the selected time period in the same journal. Selecting the 1-year option compares the metrics against other articles/reviews that were also published in the same calendar year. Selecting the 3-year option compares the metrics against other articles/reviews that were also published in the same calendar year plus the two years prior.
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations5
- Citation Indexes5
- CrossRef4
- Captures30
- Readers30
- 30
Article Description
Interferon (IFN)-β is a type I IFN commonly produced by the innate immune system in response to viral infection. IFN-β is also used for the treatment of patients with the relapsing–remitting form of multiple sclerosis (RRMS); however, IFN-β therapy is unable to confer a significant benefit for primary-progressive MS (PPMS) patients. In this study, we assessed the gene profiles of peripheral blood mononuclear cells (PBMCs) isolated from PPMS, RRMS, and healthy donors (HD) in response to IFN-β treatment in vitro to examine genetic mechanisms underlying the inadequate response of IFN-β therapy in PPMS patients. Here, we show that HLA-G was significantly less up-regulated in response to IFN-β in PBMCs from PPMS compared to those from RRMS. This data suggests HLA-G to be a possible candidate gene found impaired in IFN-β-mediated immune regulation in PPMS patients.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0165572813002889; http://dx.doi.org/10.1016/j.jneuroim.2013.10.007; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84888391352&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/24200257; https://linkinghub.elsevier.com/retrieve/pii/S0165572813002889
Elsevier BV
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