The latest in a sea of sameness is the Bristol University crap about an "on/off switch" for the immune response to MS.
Here's the full paper, published in Nature---for those who like to read published research, rather than press releases full of hyperbole and BS.
In reading the paper, we learn that this new "breakthrough" is remarkebly reminiscent of Copaxone treatment, in which killer T cells are said to be modulated 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 injected peptide epitopes, rather than intact antigens--which are said to be "more effective."
Again, all of the testing was done on the mouse model, EAE. Not humans with MS.
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, slowed cerebral blood flow and reperfusion injury in humans.
That's right!! CD4+ T cells show up after stroke, ischemia, and reperfusion injury. These cells are responding to slowed blood flow in the brain, or hypoperfusion.
Here are stroke and vascular researchers discussing CD4+ T cells and the immune reaction to stroke and vascular issues in published research. Perhaps we should let them know that stroke or reperfusion injury is an autoimmune disease that can be turned on or off!
For instance, lymphocytes from stroke survivors show more activity against myelin than the lymphocytes from patients with multiple sclerosis. In addition, myelin-reactive T cells are found in higher numbers among patients with cerebrovascular disease. These data thus provide evidence that a cellular immune response to brain antigens occurs following stroke.
These findings indicate that CD4+ and CD8+ T lymphocytes, but not B lymphocytes, contribute to the inflammatory and thrombogenic responses, brain injury, and neurological deficit associated with experimental stroke
I have a novel suggestion for researchers---why not look at the connection of MS to stroke, the vascular endothelium, CCSVI and reperfusion injury? Why not understand this cellular response in non "auto-immune" diseases?
Now that would be a REAL breakthrough,