Hi,
As someone with an intracellular infection that has been associated with auto-immune disease I thought I would take this chance to ask the good doctor about it.
I haven't looked into Hashimoto's disease much, but there does seem to be a correlation with Y. Entercolitica, and when I searched for the wrong Japanese disease I found that there is a suggested link with Kawasaki disease too.
I'm more interested in Reiter's Syndrome, though, as I seem to have had many of the symptoms of it, along with persisting IgG and IgA to Y. Enterocolitica. I would like to know what you mean by T-cell mediated rather than antibody-mediated, and why if that is true almost all the research has concentrated on the prolonged IgA antibody response rather than the T-cell response.
Also, as someone who knows the UK system, is there any way to see someone/get treatment for sub-clinical enthesitis?
Thanks,
Mark
Yersinia causes Reiter's disease, as do various other intracellular bacteria. However, there is no evidence for specific immunity against self in Reiter's so it is not an 'autoimmune disease'. I have never heard of any reliable evidence linking these organisms to diseases with true autoimmunity in the form of autoantibodies like Hashimoto's. If there was such evidence I think I would have heard about it. Kawasaki is an odd one which as far as I know is not known to be autoimmune. The term autoimmunity has been very loosely used in the past which confuses everything.
The difference between T cell mediated and antibody mediated:
The adaptive immune system that produces specific immune responses to newly encountered antigens like viruses and bacteria and gives you 'memory' for such responses involves two main types of cell: T and B. Moreover, the T cells are divided mostly into CD4 and CD8.
The job of CD4 cells is chiefly to 'help' B cells make antibody to antigens floating about between cells. The interaction involves HLA-DR and DQ molecules, which is presumably why autoantibody production is often linked to certain DR or DQ genes. The diseases of this CD4 T dependent B response are the knwon autoimmune disease like lupus, RA, coeliac, scleroderma, pernicious anaemia etc etc.
The job of CD8 T cells is to recognise viral and bacterial antigens that have got inside cells. Since viruses always get inside cells CD8s are particularly relevant to virus immunity. CD8 T cells have their antigen presented to them by any cell, not just B cells, and this involves HLA-A,B and C, not DR and DQ. Diseases associated with A,B and C genes do not show autoantibodies or in fact any evidence of autoimmunity from the T cells but seem to involve a non-specific over-reactivity of T cells. They include ankylosing spondylitis and Reiter's (B27 linked) psoriasis and its arthritis (Cw6 and B27 linked) and Crohn's or UC arthritis (B27 linked). Behcet's disease is B51 linked but may involve the interaction of HLA-B with another type of cell - NK cells.
So as far as we know Reiter's disease is an over-enthusiam of CD8 T cells (which also like to talk to CD4 T cells but not B cells) that is not truly autoimmune. In almost all cases the bacterium that starts things off either dies off or is killed by antibiotic within two or three weeks. However, the T cells do not seem to settle down. This might seem odd but in Ank spond the T cells seem to get over-reactive without any involvement of bacteria so it seems that persistent overactivity is something that can occur anyway,especially if the B is B27.