Earlier this week, I posted a variety of papers which showed a potential (according to the authors, statistically significant) relationship between haplotype and the development of chronic Lyme arthritis.
Then my attention was drawn to this 2008 paper, and I realized I shouldn't have stopped at papers in 2007 before writing my post about genetic haplotypes...
Human Homologues of a Borrelia T cell Epitope Associated with Antibiotic-Refractory Lyme Arthritis
Antibiotic-refractory Lyme arthritis, which may result from infection-induced autoimmunity, is associated with HLA-DR molecules that bind an epitope of Borrelia burgdorferi (Bb) outer-surface protein A (OspA165−173) and with T cell reactivity with this epitope. One potential mechanism to explain these associations is molecular mimicry between OspA165−173 and a self-peptide.
Here, we searched the published human genome for peptides with sequence homology with OspA165−173. The two peptides identified with the greatest sequence homology with the OspA epitope were MAWD-BP276−288, which had identity at eight of the nine core amino acid residues, and T-span758−70, which had identity at six residues. MAWD-BP mRNA was expressed by synoviocytes, while T-span7 mRNA was not. However, neither peptide bound all of the HLA-DR molecules associated with antibiotic-refractory Lyme arthritis. Among 11 patients, nine had T cell reactivity with OspA161−170, six had responses to MAWD-BP276−288, and three had reactivity with T-span758−70, but reactivity with the self-peptides was lower than that induced by the spirochetal epitope.
Thus, there remains an association between OspA165−173 and antibiotic-refractory Lyme arthritis, and infection-induced autoimmunity is an attractive hypothesis to explain this outcome. However, molecular mimicry due to sequence homology between OspA165−173 and a human peptide seems unlikely to be the critical mechanism.
I suppose I have to keep reading more research?
What's the present model for the cause of chronic Lyme arthritis these researchers are supporting again?
This work by Camp Other is licensed under a Creative Commons
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