| Title | Interferon-beta-1a treatment increases CD56(bright) natural killer cells and CD4+CD25+ Foxp3 expression in subjects with multiple sclerosis. | | Author(s) | Vandenbark AA, Huan J, Agotsch M, La Tocha D, Goelz S, Offner H, Lanker S, Bourdette D | | Institution | Neuroimmunology Laboratory, Department of Veterans Affairs Medical Center, Portland, OR, United States; Department of Neurology, Oregon Health & Science University, Portland, OR, United States; Tykeson MS Research Laboratory, Oregon Health & Science University, Portland, OR, United States; MS Center of Excellence-West, Department of Veterans Affairs Medical Center, Portland, OR, United States; Department of Molecular Microbiology & Immunology, Oregon Health & Science University, Portland, OR, United States. | | Source | J Neuroimmunol 2009 Sep 14. | | Abstract | Disease modifying effects of interferon (IFN)-beta therapy in patients with multiple sclerosis (MS) may be mediated in part through enhanced immunoregulation by the CD56(bright) subpopulation of natural killer (NK) cells and by Foxp3+ (not italicized) CD4+CD25+ regulatory T cells (Treg). We found that IFN-beta-1a(IM) treatment of relapsing-remitting (RR)MS subjects over 12months significantly increased both percentage of CD56(bright) NK cells and Foxp3 mRNA expression compared to baseline values, untreated RRMS subjects and healthy controls (HC). This striking enhancement of two prominent immunoregulatory pathways lends support to the idea that beneficial effects of IFN-beta-1a in MS include control of pernicious autoimmunity. | | Language | ENG | | Pub Type(s) | JOURNAL ARTICLE
| | PubMed ID | 19758707 |
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