Breakthrough hope for MS treatment

[MSUK]

Scientists say they have discovered how to "switch off" autoimmune diseases such as multiple sclerosis.

Researchers at the University of Bristol, who describe the work as an "important breakthrough", say it could improve the lives of millions around the world.

In their research, published today in Nature Communications, the team reveal how to stop cells from attacking healthy body tissue....... Read More - http://www.ms-uk.org/immunecells

[CureOrBust]

In the study, scientists were able to selectively target the cells that cause autoimmune disease by dampening down their aggression against the body's own tissue, while converting them into cells capable of protecting against disease

Now if the scientists could only agree on exactly which cells are causing MS.

[cheerleader]

Here's the full paper, published in Nature---for those who like to read published research, rather than press releases:
http://www.nature.com/ncomms/2014/14090 ... s5741.html

It is reminiscent of Copaxone treatment, in which killer T cells are said to be changed to helpful T cells by means of exposing them to an antigen (in Copaxone's case, that's a mimic of the proteins found in myelin basic protein---glatiramer acetate.) This particular "new breakthrough hope" therapy is going after CD4 T cells, using peptide epitopes, rather than intact antigens.

All of the testing was done on the mouse model, EAE.

As reviewed elsewhere23, 45, peptide epitopes targeting ​CD4+ T cells have distinct advantages over intact antigens, and yet the mechanism by which peptide therapy prevents and treats ongoing autoimmune and allergic diseases is poorly defined. Mucosal routes of administration have proven safe and effective in animal models of allergy and autoimmunity, but have not translated well to the clinic. Here we demonstrate that the s.c. route of administration is more effective than the i.n. route, with a 1,000-fold lower dose of antigen being effective for anergy induction when compared with previous studies17, 18. As noted17, the efficacy of tolerance induction and disease prevention depends on signal strength. In this study, all aspects of inflammatory T-cell function, including proliferation, inflammatory cytokine secretion and encephalitogenicity were suppressed, whereas the ability of cells to secrete ​IL-10 and suppress EAE increased in a dose-dependent manner. ​IL-10 clearly serves as a promising mediator of effective antigen-specific immunotherapy1, 12.

But muting or changing the inflammatory response of CD4 + T Cells isn't really explaining why they are there in the first place, or how come this exact same cellular response shows up in ischemic stroke and slowed cerebral blood flow and reperfusion injury
http://www.ncbi.nlm.nih.gov/pubmed/16247183
http://circ.ahajournals.org/content/113/17/2105.long
http://stroke.ahajournals.org/content/4 ... 1/S75.full

Nothing new under the sun,
cheer