This Is MS Multiple Sclerosis Community: Knowledge & Support

yes you are right to be sceptical I believe the statistic is something like 99% of all experiments that are successful in mice fail in humans but sometimes a little hope can bring a mood a long way .

Perhaps this may be what you are looking for...Harry

http://www.pubmedcentral.nih.gov/articl ... id=2083209

HarryZ:Not sure-think this was the Article:
http://jem.rupress.org/cgi/content/short/206/6/1303

Still EAE but different Modality.Sorry for confusion-It's getting foggy these hot/humid days!

ARTICLE
Spontaneous relapsing-remitting EAE in the SJL/J mouse: MOG-reactive transgenic T cells recruit endogenous MOG-specific B cells

Bernadette Pöllinger1, Gurumoorthy Krishnamoorthy1, Kerstin Berer1, Hans Lassmann3, Michael R. Bösl2, Robert Dunn4, Helena S. Domingues1, Andreas Holz1, Florian C. Kurschus1, and Hartmut Wekerle1
1 Department of Neuroimmunology and 2 Transgenic Service, Max Planck Institute of Neurobiology, D-82152 Martinsried, Germany
3 Center for Brain Research, Medical University of Vienna, A-1090 Vienna, Austria
4 Department of Immunology, Biogen Idec, San Diego, CA 92122

CORRESPONDENCE Hartmut Wekerle: hwekerle@neuro.mpg.de OR Florian C. Kurschus: kurschus@neuro.mpg.de

We describe new T cell receptor (TCR) transgenic mice (relapsing-remitting [RR] mice) carrying a TCR specific for myelin oligodendrocyte glycoprotein (MOG) peptide 92–106 in the context of I-As. Backcrossed to the SJL/J background, most RR mice spontaneously develop RR experimental autoimmune encephalomyelitis (EAE) with episodes often altering between different central nervous system tissues like the cerebellum, optic nerve, and spinal cord. Development of spontaneous EAE depends on the presence of an intact B cell compartment and on the expression of MOG autoantigen. There is no spontaneous EAE development in B cell–depleted mice or in transgenic mice lacking MOG. Transgenic T cells seem to expand MOG autoreactive B cells from the endogenous repertoire. The expanded autoreactive B cells produce autoantibodies binding to a conformational epitope on the native MOG protein while ignoring the T cell target peptide. The secreted autoantibodies are pathogenic, enhancing demyelinating EAE episodes. RR mice constitute the first spontaneous animal model for the most common form of multiple sclerosis (MS), RR MS.



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hehe RREAE

New mouse model gives important insights into emergence, progress of multiple sclerosis

<shortened url>

Less concentrating to understand article-easier to get the arms around.

My ?- Why these works don't make any headway or get recognition in US
research world?

Answer-BIG PHARMA!

Though I did see Novartis is getting in on this research!

Here's another:

http://www.physorg.com/news163858608.html

"Such doubly or even triply activated T cells could be the reason for the significantly greater aggressiveness of these cells", suggests Hartmut Wekerle, the head of the study. And, of course, he is already thinking one step ahead: "We must now find a way of identifying these special T cells in the patient." Based on this, treatments could be developed that specifically suppress the activity of these particularly aggressive T cells or remove them from the tissue. Such a treatment should have considerably fewer side effects than the previous, rather unspecific approaches.

Bla,Bla,Bla......

Yeah-funny RR EAE Mice

ah ha. well if i understand that at all right, if only in a simplistic way, personally i'm down with boosting my Tregs using d3, and going after these ferocious Ts that way for now at least..

JimmyLegs,

My appologies if I came off condesending!Certainly not intended.

Put in 2nd article because it is easier reading for me and doesn't give me an exaccerbation just trying to comprehend biologic gobblely-gook!

A

pshhht! not at all! it's just that i don't pretend to understand all the ins and outs of the immune system - i haven't bothered to try really.. in a very simplistic way i view it as having 'kill' and 'stop killing' signals.

the study looked like they were going to go after particularly ferocious kill cells and try to remove them, whereas i like to bolster up the 'stop killing' cells.. an immune system boost that i really feel anyone suffering from 'autoimmune' illness could use.

i think it's really a shame that some people just automatically reject 'immune system boosters' - when some of them boost important regulatory components!

hahaha!!!

Lyon, usually no one notices when I do make a post since it is so infrequent. I am on this site usually every day. I just don't post that much! My picture, well I am not sure what happened to it!

I really am still skeptical though. I hope they really start figuring out MS soon, for everyone sake.

.

this "stopping ms on mice" news was a bit puzzling. how do they cause mice those ms-like symptoms, when they don't know what triggers ms symptoms on humans? maybe this is just stupid from me..

it is NOT stupid. and it's why cures that work on artificially ms'd mice don't necessarily work on people. now if they cured mice that had something that looked like ms but they didn't know why, that might be something lol!

They physically inject the mice with a substance that causes demylination in their brains...thus the MS symptoms. But that does not mean it is the same as what causes MS in humans...in fact many scientists state the EAE in mice is not anything at all the same as MS in humans.

This why they can treat the mice and get the wonderful results they do because they know what caused their problem...unlike nobody in decades being able to determine just what causes MS to surface in humans.

Harry

and of course, if the treatment that is effective on mice turns out to be somewhat effective in treating ms in humans, then who cares about cause or prevention, we've got another treatment for sale.