Article
Impact of chemokine receptor CX3CR1 in human renal allograft rejection.
Department of Internal Medicine II-Nephrology, University Medical Center Regensburg, Franz-Josef-Strauss-Allee 11, 93053 Regensburg, Germany.
Transplant Immunology (impact factor:
1.46).
08/2010;
23(4):204-8.
DOI:10.1016/j.trim.2010.06.006
pp.204-8
Source: PubMed
-
Citations (0)
- Cited In (1)
-
Article: Fractalkine expression induces endothelial progenitor cell lysis by natural killer cells.
[show abstract] [hide abstract]
ABSTRACT: Circulating CD34(+) cells, a population that includes endothelial progenitors, participate in the maintenance of endothelial integrity. Better understanding of the mechanisms that regulate their survival is crucial to improve their regenerative activity in cardiovascular and renal diseases. Chemokine-receptor cross talk is critical in regulating cell homeostasis. We hypothesized that cell surface expression of the chemokine fractalkine (FKN) could target progenitor cell injury by Natural Killer (NK) cells, thereby limiting their availability for vascular repair. We show that CD34(+)-derived Endothelial Colony Forming Cells (ECFC) can express FKN in response to TNF-α and IFN-γ inflammatory cytokines and that FKN expression by ECFC stimulates NK cell adhesion, NK cell-mediated ECFC lysis and microparticles release in vitro. The specific involvement of membrane FKN in these processes was demonstrated using FKN-transfected ECFC and anti-FKN blocking antibody. FKN expression was also evidenced on circulating CD34(+) progenitor cells and was detected at higher frequency in kidney transplant recipients, when compared to healthy controls. The proportion of CD34(+) cells expressing FKN was identified as an independent variable inversely correlated to CD34(+) progenitor cell count. We further showed that treatment of CD34(+) circulating cells isolated from adult blood donors with transplant serum or TNF-α/IFN-γ can induce FKN expression. Our data highlights a novel mechanism by which FKN expression on CD34(+) progenitor cells may target their NK cell mediated killing and participate to their immune depletion in transplant recipients. Considering the numerous diseased contexts shown to promote FKN expression, our data identify FKN as a hallmark of altered progenitor cell homeostasis with potential implications in better evaluation of vascular repair in patients.PLoS ONE 01/2011; 6(10):e26663. · 4.09 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed.
The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual
current impact factor.
Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence
agreement may be applicable.
Keywords
174 renal graft biopsies
acute renal allograft rejection
acute tubulointerstitial
acute tubulointerstitial rejection
acute tubulus necrosis
acute vascular rejection
antibody-mediated acute rejection
CD209/DC-SIGN positive dendritic cells
cellular localization
chronic inflammatory processes
CX3CR1 positive cells
CX3CR1 positive interstitial cells
CX3CR1 positive macrophages
CX3CR1 positive staining area
human renal transplant biopsies
human renal transplantation
normal renal allograft biopsies
outcome parameters
prognostic marker
worse clinical outcome 3