Biomarker for response to interferon

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frodo
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Biomarker for response to interferon

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Semaphorin 4A as a biomarker of multiple sclerosis and neuromyelitis optica spectrum disorder

https://onlinelibrary.wiley.com/doi/abs ... cen3.12490


Abstract

Selecting appropriate treatment from the early stage of the disease is important for a better prognosis for patients with multiple sclerosis (MS). Although various disease‐modifying drugs have been approved for MS, there is no appropriate biomarker to predict treatment responsiveness. We have recently identified serum semaphorin 4A (Sema4A) as a biomarker for predicting the treatment efficacy of interferon‐β therapy. One‐third of patients with MS show high serum Sema4A levels. These patients tend to have a higher Expanded Disability Status Scale score, and possess immune characteristics of Th17‐skewing condition. Interestingly, these patients do not respond effectively to interferon‐β therapy.

However, retrospective analysis of our MS cohort showed that those with high serum Sema4A levels show a favorable response to fingolimod (FTY) therapy. Efficacy of FTY was observed even in patients who later switched to FTY due to recurrent attacks under interferon‐β therapy. Our observations suggest that FTY could be a better candidate for managing the disease activity of MS patients with high Sema4A levels. Considering the fact that the efficacy of other various disease‐modifying drugs still remains elusive among MS patients with varying Sema4A profile, further investigation is required to clarify the role of serum Sema4A as a biomarker in making an appropriate decision regarding various disease‐modifying drug choices.

For patients with neuromyelitis optica spectrum disorder, we found that a certain proportion of patients show high levels of serum Sema4A. In the present review, we discuss the current advances in the field of MS research focusing on the role of Sema4A, and further present the clinical features of neuromyelitis optica spectrum disorder patients with high Sema4A levels.
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