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T cell response to human HSP60 and yersinia 19 kDa in ankylosing spondylitis and rheumatoid arthritis: no evidence for a causal role of these antigens in the pathogenesis
  1. J Zou1,
  2. M Rudwaleit1,
  3. A Thiel2,
  4. R Lauster2,
  5. J Braun1,3,
  6. J Sieper1,2
  1. 1Department of Rheumatology, Klinikum Benjamin Franklin, Free University, Berlin, Germany
  2. 2German Rheumatology Research Centre, Berlin, Germany
  3. 3Rheumzentrum Herne, Germany
  1. Correspondence to:
    Professor J Sieper, Medical Department I, Rheumatology, University Hospital Benjamin Franklin, Hindenburgdamm 30, 12200 Berlin, Germany;
    hjsieper{at}zedat.fu-berlin.de

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The pathogenesis of two important inflammatory rheumatic diseases, rheumatoid arthritis (RA) and ankylosing spondylitis (AS), is not clear. In both diseases an immune response against an unknown autoantigen may have a crucial role.1,2 It has been repeatedly suggested that heat shock proteins (HSP) play a part in various autoimmune diseases such as RA, diabetes, and multiple sclerosis,3 based on high interspecies sequence homologies, inducible tissue expression, and a strong immunogenicity. On the other hand, some studies indicate that HSP may even be protective in arthritis.4

The 19 kDa urease β subunit of yersinia is regarded as a major immunodominant protein for both T cell and antibody responses in patients with yersinia induced reactive arthritis.5 Because 20–30% of HLA-B27+ patients with yersinia induced reactive arthritis develop the full picture of AS after 10–20 years,6 it is an obvious question to ask whether a T cell response against the yersinia-specific 19 kDa protein is also detectable in patients with AS. …

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