
they have successfully reversed ms in mice
- HarryZ
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Perhaps this may be what you are looking for...Harryjimmylegs wrote:i would definitely be interested in learning about the premise(s) on which this non-EAE murine model is founded.
http://www.pubmedcentral.nih.gov/articl ... id=2083209
- arthurherr
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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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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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- arthurherr
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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!
<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!
- arthurherr
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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
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
- arthurherr
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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!
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.
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.
- HarryZ
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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.turtle_fi wrote: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..
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