Autoimmune disease is aabnormal immune response of the body against substances and tissues normally present in the body. In other words the immune system starts attacking healthy parts of the body.
I decided to shortly write about thisdisease since it is a potential side effect following treatments with immunotherapies such as DendriticCells or anti PD1/PDL1 therapies.
It has been recently shown thatMCT1 activity is not required for lymphocyte activation, such as cytokine production, or for most normal physiological functions. However,inhibition of MCT1 during T lymphocyte activation results in selective and profound inhibition of the extremely rapid phase of T cell division essential for an effective immune response. As a result, it has been indicated that MCT1 is atarget for immunosuppressive therapy. Ref1 (As a short reminder, MCT1 is the transporter that is required from 3BP anticancer function.)
One of the well known inhibitor of MCT1 is Quercetin. Quercetin is a natural extract available at the online shops as a supplement. Other MCT1 inhibitors areLuteolin,Atorvastatin (and other statins),Diclofenac,Phloretin,Naringenin, Apigenin, Genistein, Ibuprofen, Silybin.
Great presentation onMonocarboxylate Transporters:http://www.njacs.org/wp-content/docs/2010-Spring-DrugMet-Mar.Includes list of elements interacting with MCTs and some studies of MCTs in different tissues.
Personally, I know someone who as a result of her cancer hadan auto immune diseasetriggered, targeting her eyes.Against all doctors expectations, after a few months, instead of being strongly affectedby the immune system her eyes were totally recovered. What she did during those monthswhenthe recovery has occurred, was an intensive IV Quercetin administration (1g/day). Note that this person is a medical doctor.
Therefore, whenever there is an autoimmune disease present I would consider intensive treatments with MCT1 inhibitors such as Quercetin. The best would probably be the IV administration, since the bioavailability via the oral route is reduced.