As I said, I haven't really looked into it, but when I googled Hashimoto's I found this study:
http://www.ncbi.nlm.nih.gov/pubmed/11318812
And also this one about Grave's disease:
http://www.ncbi.nlm.nih.gov/pubmed/23630351
The second one is a bit dense for me (or maybe it's the other way round), but they seem to be suggesting that this autoimmune disease is a result of molecular mimicry by Yersinia.
I don't have the medical knowledge to follow the arguments closely, but it seems to me to statements such as 'there is no evidence for specific immunity against self in Reiter's so it is not an 'autoimmune disease,' might be tautologous. Isn't the reasoning here that because there is an infectious cause in Reiter's, the immune reaction is targeting this, rather than the bodies own cells?
If that is the case, then no disease with an infectious cause can be autoimmune, and therefore as soon as you discover one, you can no longer include it in any discussion/statement about auto-immune diseases.
The same could go for molecular mimicry, if this was proven to be happening in some cases, would they no longer be considered auto-immune diseases?
Re: Reiter's syndrome, I have only read about it where it applies to Y. Enterocolitica infection, and in these cases it has been demonstrated that the immune system is responding to the ongoing presence of Y. Enterocolitica antigens. Would that make it an antibody-mediated response or a T-cell mediated response?
http://ard.bmj.com/content/59/11/914.full
I'm not trying to be difficult, I'm simply trying to make sense of what I read. I would like to be able to rely on doctors to do this for me, but after seeing an infectious disease doc in the NHS, I can only conclude that he has never read any of the Y. Enterocolitica literature. I don't blame him, as I seem to be one in a million in the UK (one report stated that the incidence rate in the UK was 0.1 in 100,000), but it does mean that I feel that I can't just rely on his opinion.
Mark