Expression of Fractalkine, CX3CR1, and Vascular Endothelial Growth Factor in Human Chronic Renal Allograft Rejection

Cao, Guorui; Liu, Yanrong; Gao, Rui; Yu, Xin; Teng, D.; Wang, J.; Li, Y.

doi:10.1016/j.transproceed.2006.06.081

Cited by 17 publications

(8 citation statements)

References 8 publications

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“…CX3CR1 is expressed on monocytes, dendritic cells, natural killer (NK) cells, as well as cytotoxic and also activated helper T cells, preferentially on T helper type 1 (Th1) -like cells, but not on B cells. [2][3][4] CX3CL1 and its receptor are implicated in several human pathological conditions including atherosclerosis, [5][6][7] agerelated macular degeneration, 8,9 allograft rejection, 10,11 rheumatic diseases 12,13 and cytomegalovirus-related vascular endothelial damage. 14 In rodent models of brain pathologies, the CX3CR1/CX3CL1 axis has been related to both pathological leucocyte migration into the central nervous system (CNS) 15,16 as well as neuroprotective mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Analyses of phenotypic and functional characteristics of CX3CR1‐expressing natural killer cells

et al. 2011

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Summary We previously demonstrated a correlation between the frequency of CX3CR1‐expressing human natural killer (NK) cells and disease activity in multiple sclerosis and showed that CX3CR1high NK cells were more cytotoxic than their CX3CR1neg/low counterparts. Here we aimed to determine whether human NK cell fractions defined by CX3CR1 represent distinct subtypes. Phenotypic and functional NK cell analyses revealed that, distinct from CX3CR1high, CX3CR1neg/low NK cells expressed high amounts of type 2 cytokines, proliferated robustly in response to interleukin‐2 and promoted a strong up‐regulation of the key co‐stimulatory molecule CD40 on monocytes. Co‐expression analyses of CX3CR1 and CD56 demonstrated the existence of different NK cell fractions based on the surface expression of these two surface markers, the CX3CR1neg CD56bright, CX3CR1neg CD56dim and CX3CR1high CD56dim fractions. Additional investigations on the expression of NK cell receptors (KIR, NKG2A, NKp30 and NKp46) and the maturation markers CD27, CD62L and CD57 indicated that CX3CR1 expression of CD56dim discriminated between an intermediary CX3CR1neg CD56dim and fully mature CX3CR1high CD56dim NK cell fractions. Hence, CX3CR1 emerges as an additional differentiation marker that may link NK cell maturation with the ability to migrate to different organs including the central nervous system.

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Section: Introductionmentioning

confidence: 99%

Analyses of phenotypic and functional characteristics of CX3CR1‐expressing natural killer cells

et al. 2011

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“…The central role of NK cells as interlinkage between innate and adaptive immune responses is increasingly appreciated (5,11,26,31). Unlike T and B lymphocytes, NK cells lyse target cells without prior antigen priming.…”

Section: Discussionmentioning

confidence: 99%

“…The interactions of activated and diseased EC with leukocytes are critical to recruiting circulating immune cells into the vessel wall destroying implanted cells and even exacerbating the initial injury. Recently, natural killer (NK) cells have been identified as pivotal host immune cells linking innate and adaptive immune responses in a variety of organ rejection reactions (5,11,26). …”

Section: Introductionmentioning

confidence: 99%

NF-κB Activity in Endothelial Cells is Modulated by Cell Substratum Interactions and Influences Chemokine-Mediated Adhesion of Natural Killer Cells

et al. 2009

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Because changes in subendothelial matrix composition are associated with alterations of the endothelial immune phenotype, we sought to understand if cytokine-induced NF-κB activity and downstream effects depend on substrate adherence of endothelial cells (EC). We compared the upstream phosphorylation cascade, activation of NF-κB, and expression/secretion of downstream effects of EC grown on tissue culture polystyrene plates (TCPS) with EC embedded within collagen-based matrices (MEEC). Adhesion of natural killer (NK) cells was quantified in vitro and in vivo. NF-κB subunit p65 nuclear levels were significantly lower and p50 significantly higher in cytokine-stimulated MEEC than in EC-TCPS. Despite similar surface expression of TNF-α receptors, MEEC had significantly decreased secretion and expression of IL-6, IL-8, MCP-1, VCAM-1, and ICAM-1. Attenuated fractalkine expression and secretion in MEEC (two to threefold lower than in EC-TCPS; p < 0.0002) correlated with 3.7-fold lower NK cell adhesion to EC (6,335 ± 420 vs. 1,735 ± 135 cpm; p < 0.0002). Furthermore, NK cell infiltration into sites of EC implantation in vivo was significantly reduced when EC were embedded within matrix. Matrix embedding enables control of EC substratum interaction. This in turn regulates chemokine and surface molecule expression and secretion, in particular of those compounds within NF-κB pathways, chemoattraction of NK cells, local inflammation, and tissue repair.

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“…61 In patients with chronic renal allograft rejection, expression of both CX3CL1 and CX3CR1 were observed in the tubulointerstitium and epithelial cell basolateral membrane. 62 Complement is associated with both antibody-mediated and non-antibody-mediated kidney diseases. 63 Recently, Thorenz demonstrated that complement 5a receptor 2 (C5aR2)-deficient mice demonstrated protection from inflammatory tissue damage and fibrosis after IR-AKI.…”

Section: Chemokines and Damage Patternsmentioning

confidence: 99%

Renal Inflammation and Fibrosis: A Double-edged Sword

Black

Lever

Agarwal

2019

J Histochem Cytochem.

131

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Renal tissue injury initiates inflammatory and fibrotic processes that occur to promote regeneration and repair. After renal injury, damaged tissue releases cytokines and chemokines, which stimulate activation and infiltration of inflammatory cells to the kidney. Normal tissue repair processes occur simultaneously with activation of myofibroblasts, collagen deposition, and wound healing responses; however, prolonged activation of pro-inflammatory and pro-fibrotic cell types causes excess extracellular matrix deposition. This review focuses on the physiological and pathophysiological roles of specialized cell types, cytokines/chemokines, and growth factors, and their implications in recovery or exacerbation of acute kidney injury.

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Expression of Fractalkine, CX3CR1, and Vascular Endothelial Growth Factor in Human Chronic Renal Allograft Rejection

Cited by 17 publications

References 8 publications

Analyses of phenotypic and functional characteristics of CX3CR1‐expressing natural killer cells

Analyses of phenotypic and functional characteristics of CX3CR1‐expressing natural killer cells

NF-κB Activity in Endothelial Cells is Modulated by Cell Substratum Interactions and Influences Chemokine-Mediated Adhesion of Natural Killer Cells

Renal Inflammation and Fibrosis: A Double-edged Sword

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