Volume 5 Supplement 2

1st Workshop of the International Society for Behçet's Disease (ISBD) on Pathophysiology and Treatment of Behçet's Disease

Open Access

Regulation of inflammatory CD28- T-helper cells by HLA class I molecules: a new cellular model for Behçet's disease?

  • C Duftner1, 1,
  • C Goldberger1,
  • E Märker-Hermann1 and
  • M Schirmer1
Arthritis Res Ther20035(Suppl 2):11

https://doi.org/10.1186/ar986

Received: 7 July 2003

Published: 9 September 2003

From immunogenetical studies we learnt that Behçet's disease (BD) is associated with HLA-B*51, and to a lesser extent with HLA-B*2702. There may even be a role of MICA genes in the pathogenesis of BD. Various of these MHC class I molecules can be recognized by NK receptors on NK and NK-T-cells independently from peptides. These NK cell receptors may be activating (DS) or inhibitory (DL). Interestingly, increased percentages of CD4+CD16+ and CD4+CD56+ T-cell subsets have already been described in BD patients.

In patients with rheumatoid arthritis and ankylosing spondylitis, unusual proinflammatory and cytotoxic CD4+ T cells marked by the lack of the costimulatory molecule CD28 express stimulatory NK cell receptors on their surface. In rheumatoid arthritis, MHC class I recognizing NK receptors are even considered as disease risk genes. In CD4+CD28- T cells from patients with ankylosing spondylitis we recently showed functional NK cell features and an enrichment of these cells in the CD4+CD25+ T-cell compartment by costimulation with HLA-B27 transfected cells.

We hypothesize that CD4+CD28- T-cells as markers of a chronic inflammatory process are also elevated in BD patients, express MHC class I recognizing NK receptors, and thus recognize HLA-B*51 via NK receptors. This mechanism could explain the chronicity of BD as an MHC class I associated disease.

Authors’ Affiliations

(1)
Department of Internal Medicine, Innsbruck University Hospital
(2)
Department of Rheumatology, University of Mainz

Copyright

© BioMed Central Ltd 2003

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