Autoimmune cross-targeting hypothesis: a virus marks the inside of a cell while a larger infection marks the outside and the combination triggers autoimmune disease. The immune system is instructed to destroy both the inside and the outside of the target.
PCBs disrupt thyroid cells by binding extra cellular transport proteins
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1257681/
It is already accepted that the PCB chemical causes disease through the disruption of thyroid hormone but how does it trigger autoimmune disease?
Could this PCB replace the larger infection, like fungal infections, in the cross-targeting hypothesis scenario? By binding to the outside of the thyroid?
Does PCB find tyroxine-binding globulin transporting the thyroid hormone out of thyroid cells and bind them up?
If this is the case then a virus is still needed to mark the inside of thyroid cells in order for Hashimoto's to be triggered.
Viral infections have been associated with Hashimoto's
http://www.ncbi.nlm.nih.gov/pubmed/20625285
PCBs disrupt thyroid cells by binding extra cellular transport proteins
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1257681/
It is already accepted that the PCB chemical causes disease through the disruption of thyroid hormone but how does it trigger autoimmune disease?
Could this PCB replace the larger infection, like fungal infections, in the cross-targeting hypothesis scenario? By binding to the outside of the thyroid?
Does PCB find tyroxine-binding globulin transporting the thyroid hormone out of thyroid cells and bind them up?
If this is the case then a virus is still needed to mark the inside of thyroid cells in order for Hashimoto's to be triggered.
Viral infections have been associated with Hashimoto's
http://www.ncbi.nlm.nih.gov/pubmed/20625285
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