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Is it time to consider rationalising IFN-ß treatment in individuals with multiple sclerosis?

Correspondence to:
Correspondence to:
G Giovannoni
Department of Neuroinflammation, Institute of Neurology, University College London, Queen Square, London, WC1N 3BG, UK; G.Giovannoni@ion.ucl.ac.uk

Keywords: interferon beta; multiple sclerosis; neutralising antibodies; MxA protein

The first 150 words of the full text of this article appear below.

In this issue Antonio Bertolotto and colleagues (see pp 1294–9),¹ use MxA mRNA expression in peripheral blood mononuclear cells (PBMCs) to assess the in vivo bioactivity of interferon-beta (IFN-ß) treatment in patients with multiple slerosis (MS). MxA transcription and translation is relatively specific for the type 1 interferons, such as interferon-alpha (IFN-) and IFN-ß, and plays an important role in the anti-viral response. MxA protein can also be used as readout for IFN-ß but with a longer temporal profile.² MxA is therefore a suitable marker to assess the bioactivity of IFNß—i.e. receptor binding, second messenger activation, gene transcription, and, in the case of MxA protein, gene translation. It appears, however, that quantitative MxA mRNA expression has some advantages over the MxA protein translation. Firstly, it has a wider dynamic range and the RT-qPCR method used to quantify its expression should be easier to standardise.³ Unfortunately, . . . [Full text of this article]