Abstract
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.
•IFN-β inducible expression profiles at baseline are similar in PPMS and RRMS•Only CBFB expression is significantly increased at baseline in RRMS versus PPMS•IFN-β-mediated HLA-G induction is significantly impaired in PPMS versus RRMS