Only problem is when you actually look at the mouse data in the majority of papers this approach actually does not do much despite what is written in the results, you only get a minor delay and small reduction in neurological signs, so dogma is maintained. Cells that transfer the disease do produce IL-17 but they may then can stop this and secrete interferon gamma. So now you have Th17-induced EAE and Th1-induced EAE, so double groan as some people now feel that you need to do both models to prove a point.
However, the IL-12 bandwagon started pharma off and so they made anti-IL12 antibodies and tried them in MS and they failed, but they were so good in EAE. But were they?. Well when they were given before disease had even started they were ace and wiped out disease. However if given to try and stop the second attack they were pretty useless, which was ignored by the dogma machine and you do not treat MS before you know you have it..at least not yet.
Now there may be some data that shows blocking IL-17 is rather rubbish as stopping mice from developing disease, it may be much better at inhibiting relapsing disease and when Th17 cells were tracked they were damaging nerves rather than initiating the initial attack, so there may be something in the Th17 story.
A trial has recently completed looking at inhibiting IL-17 in RRMSers and these people are been watched in a follow up study …..we shall see but there have been mutterings of promising results in other immune diseases.
Now the study above that was reported last year that you have asked about could have, but did not yet make a new dogma (probably because it was not born in the USA, where most -immunological-dogmas originate) and we would have had the ThGMCSF of Thcsf2 cells. GM-CSF is sometimes
used to stimulate the production/mobilize stem cells before you bone
marrow transplants and so blocking GM-CSF may have its complications,
but that is the case for any treatment. This study would suggest that blocking GM-CSF could be beneficial in RRMS.
This study indicates that cells that produce granulocyte macrophage colony stimulating factor= CSF2 are the bad boys and this is the key cytokine that drives cells to cause EAE. You don’t need IL-17 or gamma interferon to do this. IL-23 stimulated this and IL-12 blocked the development of cells making GM-SCF. They blocked GM-CSF and EAE was inhibited (although some of the effects were reported were a bit of a Shania, some looked good) so we have a new treatment option. I wonder if the anti-GM-CSF is actually affecting the macrophage/microglia?
There is clinical trial with an inhibitor of GM-CSF called MOR103 that is currently recruiting in Poland, Germany and UK, if interested press the link for details
Maybe Prof G knows more about it.