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Annals of the Rheumatic Diseases 1999;58:435-440; doi:10.1136/ard.58.7.435
Copyright © 1999 BMJ Publishing Group Ltd & European League Against Rheumatism.
Ann Rheum Dis 1999;58:435-440 ( July )

Extended reports

Ankylosing spondylitis in monozygotic twins: studies on immunological parameters Thomas Höhlera, Rosula Huga, Peter M Schneiderb, Frank Krummenauerc, Christel Gripenberg-Lerched, Kaisa Granforsd, Elisabeth Märker-Hermanna

a Medical Department of Internal Medicine, Johannes Gutenberg Universität Mainz, Mainz, Germany, b Institute of Legal Medicine, Mainz, Germany, c Institute of Medical Statistics and Documentation, Mainz, Germany, d National Public Health Institute, Department in Turku, Turku, Finland

Correspondence to: Dr T Höhler, I Medizinische Klinik und Poliklinik, Johannes Gutenberg-Universität Mainz, Langenbeckstr 1, 55101 Mainz, Germany.

Accepted for publication 9 March 1999

OBJECTIVE---To examine immunological parameters that might explain disease discordance in monozygotic twin pairs with ankylosing spondylitis (AS).
METHODS---11 monozygotic twin pairs (nine with AS, two with undifferentiated spondyloarthropathy) were investigated. The peripheral T cell receptor Vbeta repertoire was investigated using FACS analysis and 14 different Vbeta antibodies. In addition serum samples were tested for antibodies to Klebsiella pneumoniae, Streptococcus pyogenes, Candida albicans, Proteus mirabilis, and Escherichia coli. Peripheral blood lymphocyte reactivity against a number of bacteria was investigated by interferon gamma  ELISPOT assays.
RESULTS---Twins suffering from AS showed cellular hyporeactivity against K pneumoniae, S pyogenes, C albicans in the ELISPOT assays compared with healthy twins. In contrast with the antibody data, where no significant differences were observed between the two groups, AS concordant twins showed the most pronounced differences in their Vbeta repertoire on CD4+ and CD8+ lymphocytes.
CONCLUSIONS---Cellular hyporeactivity of peripheral blood cells to bacterial antigens might reflect defective T cell responses allowing bacterial antigens to persist in diseased patients. There are probably other environmental factors that influence disease concordance.


© 1999 by Annals of the Rheumatic Diseases

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