Avonex (interferon beta-1a) is made from human proteins. Interferons help the body fight viral infections.Premission to repost by Prof. Gavin Giovannoni There are some in the ME/CFS medical field that believe ME/CFS is 'MS Light' or 'Atypical MS'. Dr. Hornig alluded to this fact recently. The reason I post these articles is the fact that research in one area may spill over into another area of research or the fact that researchers reviewing a site may look at the research in another disease category that could be related to theirs and it might raise their interest level. Harking the cytokines Balasa R, Maier S, Voidazan S, Hutanu A, Bajko Z, Motataianu A. An Intricate Mechanism of Action of Avonex in Relapsing Remitting Multiple Sclerosis Patients: Variation of Serum Titre of Interleukin-17A, Interleukin-10 and Transforming Growth Factor-β.CNS Neurol Disord Drug Targets. 2015 Mar. [Epub ahead of print] INTRODUCTION: The immunopathogenesis of multiple sclerosis (MS) is a main field of research, together with the mechanism of action of most immune therapies in this disease, such as interferon beta. Interleukin (IL)-17 is considered to play a central part in the initial immune cascade in MS, though there are numerous interactions between other cytokines that might explain the heterogeneity of disease evolution and treatment response. MATERIAL AND METHODS: We tested the serum levels of IL-17A, IL-10 and transforming growth factor (TGF-β) using the enzyme-linked immunosorbent assay method in three small groups of relapsing-remitting MS patients: 10 being naïve without treatment, 10 patients receiving Avonex treatment early in the MS evolution (≤ one year from the MS onset) and 12 MS patients who received Avonex later in the disease evolution. The values were compared with those obtained from 32 healthy subjects using statistical analysis. RESULTS: In the naïve multiple sclerosis group: IL-17A values were statistically higher than among healthy subjects; IL-17A inversely correlated with MS duration; serum IL-17A negatively correlated with TGF-β. A direct correlation was found between the serum titre of IL-17A and IL-10 in the early treated multiple sclerosis group; the titre of IL-17A was significantly reduced compared with that from the late treated multiple sclerosis group. CONCLUSIONS: The role in MS pathology of IL-17A, IL-10 and TGF-β is only partially elucidated. IL-17 plays an important role in the inflammatory phase of relapsing-remitting MS and is diminished by Avonex (interferon beta-1a). Avonex (interferon beta-1a) drug is made from human proteins. Interferons help the body fight viral infections mainly if this disease modifying treatment is administered early in the evolution of MS. IL-17 is considered to be a pro-inflammatory T cell growth factor and blocking it is a thought to be a good thing. IL-10 and transforming growth factor are thought to be ant-inflammatory actors but are also pro-B cell factors. IL-17 dropped with treatment and IL-17 levels correlated with IL-10 levels. Maybe not quite what was envisioned.