http://www.msnbc.msn.com/id/44858044/ns/local_news-chicago_il/#.TpRVMXJgjCM (http://www.msnbc.msn.com/id/44858044/ns/local_news-chicago_il/#.TpRVMXJgjCM)
It's worth keeping this on the radar, but this statement makes me wonder.
QuotePreviously, the approach was used to target autoimmune diseases like Type 1 diabetes and multiple sclerosis.
AFAIK, those diseases haven't been cured. If they've tried this technique on those and it works, why aren't they treating with it? If it didn't work on those, I wonder what the chances are of it working with allergies?
Bit more here: http://io9.com/5848745/ (http://io9.com/5848745/)
The original citation is:
http://www.jimmunol.org/content/early/2011/10/04/jimmunol.1100608.abstract (http://www.jimmunol.org/content/early/2011/10/04/jimmunol.1100608.abstract)
I (personally) find this interesting:
Interestingly, Ag-SP induced Th2 tolerance was found to be partially dependent on the function of CD25+ regulatory T cells in the food allergy model, but was regulatory T cell independent in the model of allergic airway inflammation.
In other words, something that wasn't supposed to be a variable turned out to be highly correlated to the success of the response. Meh. I'm skeptical, because that often means that the underlying (supposed) mechanism isn't correct-- or at the very least, is incompletely understood.
In some conditions, in some animal models, this works. As long as nothing interferes.
What about this?
QuoteResearchers from the University of Notre Dame have announced a breakthrough approach to allergy treatment that inhibits food allergies, drug allergies and asthmatic reactions without suppressing a sufferer's entire immunological system.
The therapy centers on a special molecule the researchers designed, a heterobivalent ligand (HBL), which when introduced into a person's bloodstream can, in essence, out-compete allergens like egg or peanut proteins in their race to attach to mast cells, a type of white blood cell that is the source of type-I hypersensitivity (that is, allergy).
http://newsinfo.nd.edu/news/26774-researchers-engineer-new-way-to-inhibit-allergic-reactions-without-side-effects/ (http://newsinfo.nd.edu/news/26774-researchers-engineer-new-way-to-inhibit-allergic-reactions-without-side-effects/)
Well, it
sounds as though that could be the same thing that cromolyn has done... well,
pretty much forever. It's a mast cell stabilizer.
At least it's the same idea.
Problems with that particular approach:
- must demonstrate TRUE inertness and perfect pharmacological targeting if you plan to use a foreign molecule as a life-long treatment for a chronic condition
- most of these types of molecules have high 'off' rates-- that is, you need to redose VERY frequently, because they come off of the binding site pretty readily as soon as blood concentrations dip.
The real solution is probably targeted gene therapy which directs a patient's own body to MAKE the interfering ligand at a pretty significant rate. But there are (currently, anyway)
huge problems with using gene therapy this way, even in the very simplest models. Expression levels just aren't very predictable.