British Journal of Rheumatology 1988;27(suppl II):55—57 MOLECULAR MIMICRY: FACT OR FICTION?

Molecular studies suggest that peptide sequence similarities are present between HLA-B27 and bacteria, but the pathological mechanisms in spondyloarthropathies remain unclear. KEY WORDS. HLA-B27, Molecular mimicry. Klebsiella pneumomae, Yersima pseucioHiberculosis, Ankylosing spondylms. EVER since the discovery that HLA-B27 dominates in patients with spondyloarthropathies [1], much attention has focused on how this is related to the mechanisms of the arthritis. Two major theories have been proposed. The molecular mimicry theory postulates that there is cross-reactivity between the HLA-B27 proteins and arthritis-causing bacteria [2]. The alternate theory postulates that bacteria cause arthritis by releasing components which specifically react with the HLA-B27 host proteins. The bacterial gene encoding these releasable components reside in the plasmid(s) of bacteria colonizing almost all ankylosing spondylitis patients. At least part of it has also become integrated into the genome of the human hosts [3]. Both theories are controversial because of non-uniform reproducibility among competent laboratories. The supportive experimental evidence is based on exclusively immunological, especially serological, techniques. High affinity mono-specific antibodies are not available