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AB0148 T-cell phenotype and intracellular cytokine-production in t-cells in patients with systemic sclerosis
  1. M. Klein1,
  2. G. Almanzar1,
  3. K. Höfner1,
  4. M. Schmalzing2,
  5. S. Kleinert2,
  6. H.-P. Tony2,
  7. S. Benoit3,
  8. H. Hamm3,
  9. M. Goebeler3,
  10. M. Prelog1
  1. 1Department of Pediatrics
  2. 2Department of Internal Medicine II
  3. 3Department of Dermatology, University of Würzburg, Würzburg, Germany

Abstract

Background Systemic Sclerosis (SSc) is a disease with mostly unknown etiology. Until now, various cytokines have been identified that may play a role in the pathogenesis of the disease.

Objectives Our aim was to investigate the peripheral T-cell phenotype and intracellular cytokines in 27 SSc patients compared to 30 age-matched healthy donors (HD).

Methods Peripheral blood mononuclear cells (PBMCs) were isolated and characterized into naive (CD45RA+CD28+), central-memory (CD45RA-CD28+), memory/effector (CD45RA-CD28-) and terminally-differentiated T-cells (TEMRA) (CD45RA+CD28-) and by their intracellular cytokines (IL-17, TNFalpha, IFNgamma) using flowcytometry.

Results In 21 SSc patients with the diffuse form lower proportions of naive T-cells were found (SSc: 57.8%, HD: 64.2%). Significantly higher proportions of CCR7+ cells in CD4+ TEMRA were found in SSc patients (66.5%) compared to HD (50.4%). Patients with diffuse SSc had higher proportions of CD4+CCR6+RORgt+ T-cells (SSc: 4.8%, HD: 3.2%) with higher IL-17 production (5.6%) compared to HD (4.7%). SSc patients showed a higher production of TNFalpha (64.4%) compared to HD (54.6%), concomitantly expressing CCR7 (SSc: 46.1%, HD: 37.1%). There are nearly equal proportions of IFNgamma producing CD4 T-cells in SSc patients (10.3%) and HD (11.0%).

Conclusions Our preliminary results showed that SSc patients had a different cytokine profile in T-cells that includes abundance of CCR6+ and CCR7+ memory T-cells and more TNFalpha and IL-17 production. These findings may account for the chronic T-cell stimulation and inflammation in the pathogenesis in SSc.

Disclosure of Interest None Declared

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