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Wednesday 1 November 2017

To B, or not to B: that is the question:

Here's a pretty picture of  cells of our immune system:



First time I had an introduction to how this worked was at Cardiff in 1988. Our immune systems are truly amazing (and just a little more complex than the picture above). But I had no idea that the monoclonal antibody breakthrough at that time was being led by rituximab, (subsequently approved for use in 1997) and even less idea of the future relevance to myself. Here is the lovely Prof Steven Hauser from the US explaining the story:

https://www.youtube.com/watch?v=g83lKeSWJtc

Please bear with it (if you can spare a few minutes), he speaks clearly and and even John followed the first bit. You might want to give up after that (John fell asleep) but for me it was one of the best explanations of MS I've ever seen and how far we have come with treatments. To sum it up, MS is a B cell led disease.

Yes, T cells follow after them, join the party and cause great annoyance to the resident microglia (monocytes that settle in the brain) but the B cells started it. And we know that the memory B cell is to blame:

http://www.ebiomedicine.com/article/S2352-3964(17)30045-2/pdf

Fast forward 30 years and rituximab is at long last being used (off-label) to treat MS. Unfortunately it's too expensive for the NHS to permit off-label use. Why off-label? It was never commercially viable for Genentech (now Roche) to bother with MS clinical trials as remaining patent life expired in 2013 (Europe) and 2016 (US). So it's brother ocrelizumab ('Ocrevus') is now licensed in the US but we're still waiting in Europe. And then NICE will have to approve. I only stand any hope of receiving it if my recent MRI shows evidence of activity, allowing my kind neuro to add the magic word 'active' in front of my secondary progressive diagnosis.

But why would I want ocrelizumab when I can have off-label cladribine injections?