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2016 ; 18
(ä): 147
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Endothelial progenitor cells are differentially impaired in ANCA-associated
vasculitis compared to healthy controls
#MMPMID27338585
Wilde B
; Mertens A
; Arends SJ
; Rouhl RP
; Bijleveld R
; Huitema J
; Timmermans SA
; Damoiseaux J
; Witzke O
; Duijvestijn AM
; van Paassen P
; van Oostenbrugge RJ
; Cohen Tervaert JW
Arthritis Res Ther
2016[Jun]; 18
(ä): 147
PMID27338585
show ga
BACKGROUND: Endothelial progenitor cells (EPC) are of major importance in
vascular repair under healthy circumstances. Vascular injury in need of repair
occurs frequently in ANCA-associated vasculitis (AAV). A specialized T cell
subset enhancing EPC function and differentiation has recently been described.
These angiogenic T cells (Tang) may have an important impact on the vascular
repair process. Therefore, the aim of our study was to investigate EPC and Tang
in AAV. METHODS: Fifty-three patients suffering from AAV and 29 healthy controls
(HC) were enrolled in our study. Forty-four patients were in remission, nine
patients were in active state of disease. Patients were either untreated or were
under monotherapy with low-dose steroids (max. 5 mg/day) at the time of sampling.
Circulating EPC and Tang were determined by flow cytometry (FACS). The functional
capacity of EPC was assessed by established cell culture methods. RESULTS:
Circulating EPC were significantly decreased in AAV as compared to HC. The
capacity of EPC to differentiate and proliferate was differentially impaired in
patients as compared to HC. The outgrowth of endothelial colony-forming cells
(ECFC) was severely decreased in patients whereas colony-forming
units-endothelial cell (CFU-EC) outgrowth was unaffected. ECFC and CFU-EC
differentiation was strictly T cell-dependent. Patients with a relapsing disease
course had an impaired ECFC outgrowth and expansion of Tang as compared to
patients with a stable, nonrelapsing disease. CONCLUSIONS: The differentiation
process of EPC is impaired in AAV. This may favor insufficient vascular repair
promoting a relapsing disease course. Finally, these factors may explain a higher
cardiovascular morbidity as has been previously documented in AAV.