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Fractalkine expression in human renal inflammation
Paul Cockwell1, Srabasti J Chakravorty, John Girdlestone
1Department of Renal Immunobiology, Division of Medical Sciences, Medical School, University of Birmingham, Birmingham, UK. paul.cockwell@university-bim.wmids.nhs.uk
The Journal of Pathology
|December 19, 2001
Summary
Fractalkine directs immune cell movement in kidney inflammation. This study shows fractalkine is expressed in diseased kidney areas, suggesting its role in recruiting mononuclear cells to inflamed renal tissue.
Area of Science:
- Nephrology
- Immunology
- Cell Biology
Background:
- Immune and inflammatory human renal diseases involve significant mononuclear cell infiltration.
- Chemokines, produced locally, guide these cells to inflamed areas.
- Fractalkine is a unique cell-surface chemokine with potent immune cell adhesion and migration properties.
Purpose of the Study:
- To investigate the expression and distribution of fractalkine in human renal inflammation.
- To determine fractalkine's role in directing mononuclear cell infiltration in kidney diseases.
Main Methods:
- In situ hybridization and immunohistochemistry were used on renal biopsies.
- Evaluated samples from patients with vasculitic glomerulonephritis and acute renal allograft rejection.
- Compared findings with non-inflammatory glomerulonephritis and normal kidney tissue.
Main Results:
- Fractalkine mRNA was highly expressed in diseased kidney compartments (glomerular or tubulointerstitial) and vascular sites.
- Increased fractalkine mRNA expression was observed in tubular epithelial cells during acute renal allograft rejection.
- Fractalkine expression correlated with macrophage (CD68+) and T cell (CD3+) infiltrates, but not by infiltrating leukocytes themselves.
Conclusions:
- Fractalkine is predominantly expressed in inflamed renal tissue, particularly near affected areas.
- The expression pattern suggests fractalkine plays a significant role in directing mononuclear cell infiltration in human renal inflammation.
- Fractalkine is a key mediator in the inflammatory response within the kidney.