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Two kinds of Multiple Sclerosis, two different responses to beta-interferon, Stanford study shows - http://www.msrc.co.uk/index.cfm?fuseact ... pageid=722

Sqiffy thanks for this post, very very interesting. I always wondered why I actually got worse when on interferons. Thanks for posting the link.

That's OK Wonderful, what MSRC are here for Think this is goign to be a very BIG story this week....... lots of implications and things to mull over and to be raised........

I was going to link to this article

Hi Why, it is the same story, it is just MSRC broke it first last night

That is true, but the good thing about the Globe link, is that people can leave a comment. I left a very messy one! No editing button, oops. The Globe has not reported on this, so leaving comments is a good way to reach people who will read the article just because it is MS related....just trying to spread the news, even though it is old to us, there are plenty of other people to reach out to.

IL-17 family members belong to a distinct category of cytokines that coordinate local tissue inflammation by inducing the release of pro-inflammatory and neutrophil-mobilizing cytokines. The importance of the IL-17 family in inflammatory and autoimmune disease is becoming increasingly apparent. IL-17F is a recently discovered member of the IL-17 family that has a number of biological activities through induction of various cytokines, chemokines, and mediators.

http://www3.interscience.wiley.com/jour ... 3/abstract

The researchers at Stanford find that pwMS with higher levels of IL-17F in their blood don't "respond" to beta interferon as well as people with lower levels of IL-17F.

What does "respond" to beta interferon actually mean? People with lower levels of IL-17F may naturally have less relapses than people with higher numbers. They may have a more mild disease course. How can these doctors claim they are responders to beta interferon?

My question is....what is creating higher levels of IL-17F in the first place? Dr. Dake has come forward with work that confirms Dr. Zamboni's studies. Venous insufficiency MIGHT begin the inflammatory cycle, inducing the release of pro-inflammatory cytokines. In the EAE model, it would be an outside antigen, which is...what? Injections of myelin?

cheer

Joan what are you trying to say by stating that Dr. Dake has come forward with work that confirms Dr. Zamboni's study? If you are saying he confirmed that CCSVI may occur somewhere in the MS process you are correct. The Buffalo Study also seemed to confirm this hypothesis on a much larger scale although it does not show the 100% correlation Zamboni initially believed to be the case. To clarify, NO one has proved that venous insufficiency begins the inflammatory cycle. In fact the Buffalo findings, if one looked at the results critically instead of emotionally, seem to say the opposite. It seems that people with a CIS had a much lower rate of CCSVI than people who had MS for a number of years. Please reread the Wall Street Journal article again because I do not see where Dr. Dake gets denigrated. Of course since the CCSVI theory broke any questions or criticisms of Zamboni or Dake have been labeled as attacks so it does not surprise me that this article would be looked at in this light.

scorp...you're absolutely right. my bad.
There's a lot of background info on this one, and I didn't preface my post with that fact.

Anyhow...my main question is- (and I have edited the rant)

Is the fact that some pwMS have more IL-17F really that big a discovery? In mice with EAE, the more IL-17F in the blood, the worse the EAE gets when exposed to beta interferon. Obviously, not good...for mice with EAE, and potentially pwMS and high IL-17F levels.

How does that translate into pwMS that have lower IL-17F levels being better "responders" to beta interferon? Because they maybe have less relapses? How can researchers be sure that is due to the beta interferon? And what causes the higher levels of IL-17F in humans? That's what I'm really asking. Is this a big deal? Someone explain why-
cheer

How can these doctors claim they are responders to beta interferon?

I suppose if one does worse on interferon, up until now, the finger of blame has not been pointed at interferon. People who did not respond to interferon have been called 'interferon-failures' whereas with this info perhaps some neuros will start to see interferon as an active agent in disimproving the disease course for some MS'ers, rather than the MS over-riding the interferons' supposedly positive effect - at least this study shows that in some people interferons are actually a negative effect on the disease course....well, in mice with EAE.

I know in my case, on interferon, I was considered 'worsening RR-MS' and my neuro wanted to give me chemo. Once I came off it and went on Copaxone I went back to just RR-MS. Interferon seemed to be 'upping' the number of relapses to 4 per year.

I'd be interested to know if high levels of IL-17F correlate to any types of MS, or specific types of disease course.