Autoimmune Cross-targeting hypothesis: 2 simultaneous infections on one target triggers autoimmunity. One infection is on the outside of the target cell and one infection is on the inside of the target. The partners of the infection can vary but the inside and outside paradigm is what triggers the autoimmune response that results in the development of autoimmune disease.
This is one of the few times where the type of infection has slightly altered the type of autoimmune disease. Apparently which virus on the inside doesn't matter but the type antibody attack on the outside of the thyroid matters. Previously Hashimoto's anti-TPO antibodies was connected to the peroxidase spewed out by fungal infections. In the case of Graves disease Yersinia creates anti-thyroid antibodies against TSH receptors. The result is 2 different types of autoimmune thyroid disease.
Graves may or may not be cross-targeting autoimmunity. Since the goiter of graves is not the destruction of the thyroid rather a swelling due to over activation of the receptors. Cross-reactivity of the antibodies are stimulating the receptors causing the thyroid to over produce. The thyroid is not attacked by the immune system.
Thyroid medication for graves can however trigger the immune system to attack resulting in Hashimoto's. http://www.ncbi.nlm.nih.gov/pubmed/2434520
Which leads me to believe that true autoimmune cross-targeting leads to the destruction of the tissue by the immune system.
Multiple viruses can infect the thyroid triggering cross-targeting autoimmunity: enteroviruses, flaviviruses, entroviruses, retroviruses and even herpes viruses. (or medication can mark the inside of the thyroid as foreign instead of the virus)
Only yersinia seems connected to Graves as the outer infection. The yersinia connection is well documented and accepted. The question now is: can other infections like e.coli or mycoplasmas create the TSH receptor antibodies?
For the Graves disease type of thyroid autoimmune disease only Yersinia infections appear to trigger the antibodies against the TSH receptor
coxsackie, graves and y.entercolitica
http://www.ncbi.nlm.nih.gov/pubmed/9561915
graves and y.enterocolitica
http://www.ncbi.nlm.nih.gov/pubmed/23630351
http://www.ncbi.nlm.nih.gov/pubmed/12193307
http://www.ncbi.nlm.nih.gov/pubmed/2083529
Graves' disease and immune thrombocytopenia (ITP)
http://www.ncbi.nlm.nih.gov/pubmed/26278293
thrombocytopenia and yersinia
http://www.ncbi.nlm.nih.gov/pubmed/3993437
haemolytic uraemolytic syndrome and yersinia
http://www.ncbi.nlm.nih.gov/pubmed/3153031
http://www.ncbi.nlm.nih.gov/pubmed/1936156
reactive arthritis and yersinia
http://www.ncbi.nlm.nih.gov/pubmed/3662638
note my earlier post considering yersinia and fish allergy
http://angelabiggs.blogspot.com/2015/04/fish-allergy-and-yersinia-infections.html
spirochetes could do this too
Thrombocytopenia and spirochetes
http://www.ncbi.nlm.nih.gov/pubmed/7044515
spirochetes and yersina share thyroid antigens
http://www.ncbi.nlm.nih.gov/pubmed/16571084
http://www.ncbi.nlm.nih.gov/pubmed/15671776
relationship between graves disease and h.pylori but not hoshimotos
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3296983/
For graves disease to become a Cross-targeting autoimmune disease a virus or medication must mark the inside as foreign and the immune system must catch the antibody binding the receptor quickly before it disappears.
Graves and hepatitis C
http://www.ncbi.nlm.nih.gov/pubmed/25603854
http://www.ncbi.nlm.nih.gov/pubmed/10426583
Coxsackie is a culprit for goiter
http://www.ncbi.nlm.nih.gov/pubmed/2853353
Note that typically the list of viruses trigger autoimmunity is smaller but the thyroid has a variety of receptors thus a larger group of viruses.
Cross-reactivity is when an antibody binds not just the antigen(sequence) of the infection but an antigen of self because the protein is either the same or similar enough. Our own body has accidentally become labeled with infection flags.
Graves is when the receptor is not just marked by an antibody but activated by it. The reason autoimmune attack on the thyroid is not triggered as often may do with the "activation" and quick cycling of the receptor away from the membrane surface. The immune system has less chance to see it. Hashimoto's can result but the "window" is smaller.
This is one of the few times where the type of infection has slightly altered the type of autoimmune disease. Apparently which virus on the inside doesn't matter but the type antibody attack on the outside of the thyroid matters. Previously Hashimoto's anti-TPO antibodies was connected to the peroxidase spewed out by fungal infections. In the case of Graves disease Yersinia creates anti-thyroid antibodies against TSH receptors. The result is 2 different types of autoimmune thyroid disease.
Graves may or may not be cross-targeting autoimmunity. Since the goiter of graves is not the destruction of the thyroid rather a swelling due to over activation of the receptors. Cross-reactivity of the antibodies are stimulating the receptors causing the thyroid to over produce. The thyroid is not attacked by the immune system.
Thyroid medication for graves can however trigger the immune system to attack resulting in Hashimoto's. http://www.ncbi.nlm.nih.gov/pubmed/2434520
Which leads me to believe that true autoimmune cross-targeting leads to the destruction of the tissue by the immune system.
Multiple viruses can infect the thyroid triggering cross-targeting autoimmunity: enteroviruses, flaviviruses, entroviruses, retroviruses and even herpes viruses. (or medication can mark the inside of the thyroid as foreign instead of the virus)
Only yersinia seems connected to Graves as the outer infection. The yersinia connection is well documented and accepted. The question now is: can other infections like e.coli or mycoplasmas create the TSH receptor antibodies?
For the Graves disease type of thyroid autoimmune disease only Yersinia infections appear to trigger the antibodies against the TSH receptor
coxsackie, graves and y.entercolitica
http://www.ncbi.nlm.nih.gov/pubmed/9561915
graves and y.enterocolitica
http://www.ncbi.nlm.nih.gov/pubmed/23630351
http://www.ncbi.nlm.nih.gov/pubmed/12193307
http://www.ncbi.nlm.nih.gov/pubmed/2083529
Graves' disease and immune thrombocytopenia (ITP)
http://www.ncbi.nlm.nih.gov/pubmed/26278293
thrombocytopenia and yersinia
http://www.ncbi.nlm.nih.gov/pubmed/3993437
haemolytic uraemolytic syndrome and yersinia
http://www.ncbi.nlm.nih.gov/pubmed/3153031
http://www.ncbi.nlm.nih.gov/pubmed/1936156
reactive arthritis and yersinia
http://www.ncbi.nlm.nih.gov/pubmed/3662638
note my earlier post considering yersinia and fish allergy
http://angelabiggs.blogspot.com/2015/04/fish-allergy-and-yersinia-infections.html
spirochetes could do this too
Thrombocytopenia and spirochetes
http://www.ncbi.nlm.nih.gov/pubmed/7044515
spirochetes and yersina share thyroid antigens
http://www.ncbi.nlm.nih.gov/pubmed/16571084
http://www.ncbi.nlm.nih.gov/pubmed/15671776
relationship between graves disease and h.pylori but not hoshimotos
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3296983/
For graves disease to become a Cross-targeting autoimmune disease a virus or medication must mark the inside as foreign and the immune system must catch the antibody binding the receptor quickly before it disappears.
Graves and hepatitis C
http://www.ncbi.nlm.nih.gov/pubmed/25603854
http://www.ncbi.nlm.nih.gov/pubmed/10426583
http://www.ncbi.nlm.nih.gov/pubmed/12729321
http://www.ncbi.nlm.nih.gov/pubmed/21928702
http://www.ncbi.nlm.nih.gov/pubmed/16025878
viruses and autoimmune thyroid disease
http://www.ncbi.nlm.nih.gov/pubmed/19138419
http://www.ncbi.nlm.nih.gov/pubmed/21928702
http://www.ncbi.nlm.nih.gov/pubmed/16025878
viruses and autoimmune thyroid disease
http://www.ncbi.nlm.nih.gov/pubmed/19138419
http://www.ncbi.nlm.nih.gov/pubmed/2853353
Note that typically the list of viruses trigger autoimmunity is smaller but the thyroid has a variety of receptors thus a larger group of viruses.
Cross-reactivity is when an antibody binds not just the antigen(sequence) of the infection but an antigen of self because the protein is either the same or similar enough. Our own body has accidentally become labeled with infection flags.
Graves is when the receptor is not just marked by an antibody but activated by it. The reason autoimmune attack on the thyroid is not triggered as often may do with the "activation" and quick cycling of the receptor away from the membrane surface. The immune system has less chance to see it. Hashimoto's can result but the "window" is smaller.
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