Peripheral blood T cell expansions in patients with Behcet's disease

Esin S., Gul A. , Hodara V., JeddiTehrani M., Dilsen N., Konice M., ...More

CLINICAL AND EXPERIMENTAL IMMUNOLOGY, vol.107, no.3, pp.520-527, 1997 (Journal Indexed in SCI) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 107 Issue: 3
  • Publication Date: 1997
  • Doi Number: 10.1046/j.1365-2249.1997.d01-947.x
  • Page Numbers: pp.520-527
  • Keywords: T cell receptor, autoimmunity, V beta gene segment, J beta gene segment, Behcet's disease, HEAT-SHOCK PROTEIN, GENE USAGE, RECEPTOR, GAMMA, PEPTIDES, AUTOIMMUNITY, ASSOCIATION, RECOGNITION, ANTIBODIES, EXPRESSION


Behcet's disease (ED) is a chronic multisystemic inflammatory disorder characterized mainly by recurrent oral and genital aphthous ulcerations and uveitis. Etiology and pathogenesis of ED remain unknown. T cell receptor (TCR) V alpha/N beta gene product expression as well as J beta gene segment expression in peripheral blood of BD patients were analysed to investigate the possible role of T lymphocytes in the etiopathogenesis of BD. Flow cytometry with 12 TCR V-specific MoAbs was used for TCRV analyses. J beta gene segment usage by T cell populations expressing certain V beta s was determined by polymerase chain reaction (PCR) technique with V beta- and C beta-specific primers, Southern blotting of PCR products, and subsequent hybridization with radiolabelled J beta gene segment-specific probes. Although 13 of the 23 ED patients exhibited increases in expression of one or more TCR V-gene products, only expansions among the CD4(+) T cell subset were significantly more frequent in ED patients (7/23) compared with healthy controls (0/15) (P = 0.019). Six out of eight cases followed for up to 20 months had at least one expansion correlated with disease activity. A strict preference for particular J beta gene segments implicating clonality was apparent in all analysed T cell expansions and correlated well with disease activity. These results suggest a possible involvement of antigen-specific T lymphocytes in the pathogenesis of ED.