Endothelial dysfunction is independent of inflammation and altered CCR7 T cell expression in patients with ankylosing spondylitis.

Objectives: The accumulation of CCR7 (chemokine receptor 7) positive cells in the vessel wall may be involved in endothelial dysfunction and subsequent accelerated atherogenesis. CCR7 plays a crucial role in T cell and monocyte migration/homing and in priming of naive T lymphocytes in non-lymphoid tissues in chronic inflammatory diseases. Our objective was to investigate the endothelial function and inflammation-driven expression of CCR7 on T lymphocytes in patients with ankylosing spondylitis (AS).

Methods: We performed flow cytometry to assess the distribution of peripheral blood T cell subpopulations in the context of serum inflammatory markers (TNF-α, IL-6, sICAM-1) and asymmetric dimethylarginine (ADMA) in 38 patients with AS with active disease, and in 20 healthy controls.

Results: Patients with AS demonstrated higher ADMA (0.74±0.2 μmol/l vs. 0.64±0.15 μmol/l; p=0.03), as well as elevated inflammatory markers (TNFα, IL-6, sICAM-1) and increased proportions of circulating CCR7-positive lymphocytes largely attributable to elevated CD8+ naive T cells (47.1±17 vs. 34.3±13.1%; p=0.005). However, ADMA did not correlate with either CCR7-positive lymphocytes or inflammatory markers.

Conclusions: We found an increased percentage of peripheral CCR7 T cells accompanied by endothelial dysfunction in patients with AS. The lack of direct associations between ADMA and inflammation may suggest the presence of other pathogenic mechanisms contributing to accelerated atherogenesis and increased cardiovascular risk in AS.