Does any one in the know, reading the blog, care to comment?
Havrdová E, Belova A, Goloborodko A, Tisserant A, Wright A, Wallstroem E, Garren H, Maguire RP, Johns DR. Activity of secukinumab, an anti-IL-17A antibody, on brain lesions in RRMS: results from a randomized, proof-of-concept study. J Neurol. 2016; 263:1287-95.
So amazing…I hear the immunologists say…but if we put it in the context of beta interferon over 24 weeks.
There was a 68% reduction in the mean cumulative number of new gadolinium lesion with subcutaneous interferon beta-1a (P<0.001).
Efficacy and safety of subcutaneous interferon β-1a in relapsing-remitting multiple sclerosis: further outcomes from the IMPROVE study.J Neurol Sci. 2012 Jan 15;312(1-2):97-101.
Contrast this to ocrelizumab with a 90-95% reduction of MRI lesion in the phase II.
Should we get more excited about a 67% reduction?
An annualised relapse rate of 0.4 verses 0.15 seen with alemtuzumab, cladribine and ocrelizumab to name three active agents. Yes I know they are different trial conditions and duration.
Meanwhile it seems that plans have been quietly shelved to do the next MS study, with the more effective anti-IL17. We are years down the line and nothing.
But what happened in animals, where the TH17 dogma was generated?
What happens when you block IL-17 in EAE?
IL-17 Knockout (100% get EAE and the severity is dropped severity a bit……..Hardly impressive.
Don’t believe it? Try another study
and antibodies
I could go on and on
Simple answer is, it isn’t very impressive in acute EAE
However, remember anti-IL-17 is not inert and it acts of B cells:-).
Th17 may create B cell aggregates in EAE
However, it is important to look at the data and not the rhetoric🙂
*The Bees knees = best thing
It would be great, if you provided the citations of the papers from which you used the figures as well.