Background Recent evidences underlined the central role of T-cells in the pathogenesis of Systemic Lupus Erythematosus (SLE) and in its cardiovascular complications.¹ CD3 +CD31+CXCR4+angiogenic T-cells (Tang) have been identified as a T-cell subtype involved in the repair of damaged endothelium cooperating with endothelial progenitor cells.² Tang were described as selectively expanded in the circulation of systemic sclerosis patients displaying peripheral vascular complications, as a reaction to an inefficient angiogenesis.³ Not much information is available on Tang in a SLE patients: in a recent study the percentage of circulating CD8 +Tang, but not CD4 +Tang, was higher in SLE than in healthy controls.⁴ However, in this study SLE patients with hypertension, dyslipidemia or smoking habit, factors which may influence Tang counts, were not excluded.

The aim of this study was to characterise Tang in a cohort of patients with SLE without known cardiovascular risk factors.

Methods Twenty female SLE patients with a recent disease onset (<5 years) and without traditional cardiovascular risk factors or previous events (age: median value=43 [25th-75th percentile=27–54] years) and 18 healthy controls (age: 40 [32–54] years) were enrolled.

Phenotypic analysis of peripheral Tang lymphocytes was made by flow-cytometry.

Disease activity was evaluated by SLEDAI-2K score.

Results SLE patients were divided in two groups according with disease activity. Patients with SLEDAI-2K equal or higher than 6 were defined as patients with high disease activity (n:5). They had a lower percentage of circulating Tang in comparison with healthy controls (10 [8–15] vs 16 [14–23]% of CD3 +T cells, p=0.04). The result was confirmed in absolute number (83 [60–103] vs 242 [165–328] cell/microliter, p=0.04). SLE patients with low disease activity had levels of Tang which were intermediate between, and not significantly different from, healthy controls and patients with high disease activity.

Conclusions Tang were reduced in our patients with active SLE, and no known cardiovascular risk factors, suggesting that this reduction was directly explained by disease activity.

References

1. . Mak A. J Immunol Res2014.

2. . Hur J. Circulation2007.

3. . Manetti M. PLoS One2017.

4. . Miao J. Mediators Inflamm2016.