Potential New Treatment for Autoimmune Diseases.



For generations, doctors have been trying to understand autoimmune diseases and how to treat them.
More than 80 such diseases affect Canadians, such as rheumatoid arthritis and type one diabetes, but new research from the University of Calgary could provide a solution.
Doctor Pere Santamaria with the Cumming School of Medicine says, right now, these diseases are so hard to treat because they involve some of the patient’s white blood cells attacking the body.
“It’s impossible to distinguish these bad white blood cells from the good white blood cells that populate the immune system.”
So, his team has developed a new class of drugs that use a naturally occurring process to treat them.
They have already had great success with type one diabetes, and a couple of other diseases.
“With animals that have a form of disease that’s similar to multiple sclerosis in humans, the animals are paralyzed in cages, they can’t walk, they can’t run. We treat them with these drugs and they’re running around,” continues Dr. Santamaria.
This brand new discovery uses a naturally occurring process to turn bad white blood cells good again, to stop the affects of these diseases.
At this point, only dangerous, toxic drugs can be given to patients, further compromising their immune system.
These drugs act completely different than what is available now.
“They do not eliminate anything, they enhance something that is wired into our immune system to protect us from these diseases. So it’s a completely different way to look at autoimmune diseases and how to treat them,”
says Santamaria.
The drugs can also be tailored for use on about 80 different autoimmune diseases, by making only a small change.
“It’s basically a one-for-all type of approach,” he concludes.
Dr. Santamaria hopes to start clinical trials in the next three years.


For those that want the full scoop...From Nature:

Regulatory T cells hold promise as targets for therapeutic intervention in autoimmunity, but approaches capable of expanding antigen-specific regulatory T cells in vivo are currently not available. Here we show that systemic delivery of nanoparticles coated with autoimmune-disease-relevant peptides bound to major histocompatibility complex class II (pMHCII) molecules triggers the generation and expansion of antigen-specific regulatory CD4+ T cell type 1 (TR1)-like cells in different mouse models, including mice humanized with lymphocytes from patients, leading to resolution of established autoimmune phenomena. Ten pMHCII-based nanomedicines show similar biological effects, regardless of genetic background, prevalence of the cognate T-cell population or MHC restriction. These nanomedicines promote the differentiation of disease-primed autoreactive T cells into TR1-like cells, which in turn suppress autoantigen-loaded antigen-presenting cells and drive the differentiation of cognate B cells into disease-suppressing regulatory B cells, without compromising systemic immunity. pMHCII-based nanomedicines thus represent a new class of drugs, potentially useful for treating a broad spectrum of autoimmune conditions in a disease-specific manner.


For people who are ready to get started increasing Tregs right away...From Selfhacked. I highly recommend reading the whole post here.
Top 8 Picks to Increase Tregs



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Wow, that's a lot of 'common' causes of brain fog. I had no idea so many people with different issues were stuggling with brain fog. Guess we aren't alone. :)


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Reactive Oxygen Species Prevent Imiquimod-Induced Psoriatic Dermatitis through Enhancing Regulatory T Cell Function

For the molecular mechanism that may link ROS level and Treg function, we investigated the expression of an immunoregulatory enzyme, indoleamine 2,3-dioxygenase (IDO) which is induced by ROS, in PD lesions. Taken together, it was implied that appropriately elevated levels of ROS might prevent psoriasis through enhancing IDO expression and Treg function.
Hopefully this research will encourage further research to discover more autoimmune antibodies/antigens (bit autoimmune antibody binds to). Even if only a small percentage of cases of ME/CFS are an autoimmune form, those cases may help to give insight into other forms of the disease. I think Angela Vincent's laboratory in Oxford University UK are doing some work on autoimmune antibodies in ME/CFS.
Random thought - is it now possible to create an animal model of an autoimmune disease using the antigen (and nanoparticle) and then turn it off again by adding the Major Histocompatibility Complex?

Folks in Bristol University UK published research in September 2014(?) showing that you can turn off autoimmune disease i.e. if you have the antigen. So I'm not sure whether/how this moves the story on i.e. I'm guessing that you need to have the antigen to adopt the Bristol/Canadian approach. Still the replication of research is welcome and the fact that they're both finding possible treatment options which are not based on immune suppression (such as steroids) is welcome.

Here's hoping this will encourage further research!

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