Hypothesis
HLA-B27 associated spondyloarthropathy, an autoimmune disease
based on crossreactivity between bacteria and HLA-B27?
J H Ringrose
Academic Medical
Centre, University of Amsterdam, Department of Medical Microbiology,
the Netherlands
Correspondence to: Dr J H Ringrose, Department of Medical Microbiology, Academic Medical Centre, AMC L1-160, PO Box 22660, 1100 DD Amsterdam, the Netherlands.
Accepted for publication 30 March 1999
Most autoimmune diseases are associated with certain HLA types.
Therefore, spondyloarthropathies (SpA) strongly associated with
HLA-B27, are also often classified as autoimmune diseases. This study
questions whether SpA indeed fulfils the criteria of an autoimmune
disease. The Medline database was searched for all reports between 1966 and April 1998 on the presence of autoimmune reactivity in SpA
patients. This search yielded 45 articles on this subject. Only eight
articles study T cell reactivity. Twelve reports were found on the
assessment of antibodies crossreacting between bacteria and HLA-B27. In
the 45 studies demonstrating autoimmune reactions in SpA patients
proper controls matched for HLA-B27, sex and age were nearly always
lacking. Therefore, it is concluded that the frequency of increased
autoreactivity in sera from patients and controls is not significantly
different, and that this lack of autoreactivity does not justify
classification of SpA as an autoimmune disease. As crossreactive
antibodies against bacteria and HLA-B27 were equally present in sera
from patients and controls, the pathogenetic significance of molecular
mimicry between various bacteria and HLA-B27 is questionable.
Furthermore, the regions of the B27 molecule that are supposed to be
crossreactive with bacteria, differ in one or more amino acids among
the distinct B27 subtypes. Although these differences strongly
influence the binding of antibodies to the B27 molecule, there was no
relation between the degree of crossreactivity of certain subtypes and the association of these subtypes with SpA. In conclusion, there is no
evident proof that SpA is an autoimmune disease attributable to
crossreactivity between bacteria and HLA-B27.
© 1999 by Annals of the Rheumatic Diseases
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