Not sure how your friend came up his summary as it appears to be totally opposite to what the investigators determined.

This is what the scientific experts concluded in the paper "Interpretation
Natalizumab increases cellular immune responses specific to viruses and myelin proteins in the peripheral blood after 1 year, without evidence of viral reactivation."

Will have to send your info to my friend and see what comes back. This stuff is beyond my understanding.

Harry

This is what I got back and it kind of makes sense to me.

Harry
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There is difference between cellular immune response and humoral immune response. Cellular immune response, also referred to as a Th1 response, is a cell mediated response indicative of inflammation and cell destruction. Which is what Tysabri increased. The humoral response, which the article states remained unchanged, is a Th2 response in which the immune cells produce antibodies to viruses to destroy and prevent further and future infection in the body by the viruses. The article states that the humoral response was unchanged yet the cellular immune response was increased. This indicates that the virus is proliferating and causing cell destruction and the immune system isn't fighting back by producing antibodies. Thus, this is a silent destruction going on and the reason that they say there is no evidence of reactivation is because the body isn't launching an attack. This attack would normally produce the outward symptoms and reactivation is often measured by the number of antibodies being produced by the body.

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The explanation still makes no sense to me. The summary to me states that cellular immune response to viruses is increased in the blood which makes sense given Tysabri's mechanism of action of confining antibodies to the bloodstream.

Obviously the problem with PML is that the virus is out of the bloodstream and into the CNS and Tysabri keeps antibodies out of the CNS.

I guess the question remains is do you really want viruses (not just JCV) proliferating in your bloodstream which Tysabri seems to allow. Maybe some very scientific person will see this and comment.

Harry

I guess you didn't understand my reply. The abstract you referenced states that the immune response is increased in the bloodstream. There is no viral proliferation in the bloodstream and won't be because of the increased immune response there.

The issues with Tysabri relate to infections outside of the bloodstream - I believe the only safety signal that has been confirmed through commercial use is PML.

harry, please remember that this thread is for those who are using or inquiring about tysabri

you have been asked before to start new thread for comments or critique

Hi all Wondering about other experiences with Ty. I tried copax, but late in my 2nd year my IPIRs got too frequent. I've been on Rebif for almost a year, and then had an allergic reaction to the med this past week.

My doc thinks that Ty should be the next step, and I'll be discussing it with the hubby tonight since we're a united front on the MS stuff - but also wanted to get other opinons. Been reading some of what's been posted, so it's going to be an interesting decision ahead. The above issues with the other DMD's as well as other meds make me leary to try this, but trying to decide whether or not to give this a shot.

Thanks for listening.

Chemar,

Yes, I am aware that this thread is for those who are using or inquiring about Tysabri. But I believe it was Natalie who mentioned the Lancet article and others who wanted to understand what this article possibly meant.

I would have thought that anyone who was considering using Tysabri would want to know what the Lancet article was stating and thus my comments from someone who was involved in MS research. If this was outside the boundaries of the thread, then I do apologize.

Harry