Journal
KIDNEY INTERNATIONAL
Volume 85, Issue 5, Pages 1123-1136Publisher
ELSEVIER SCIENCE INC
DOI: 10.1038/ki.2013.522
Keywords
adhesion molecule; crescentic glomerulonephritis; endothelium; macrophage
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Funding
- Institut National de Sante et de la Recherche Medicate (INSERM)
- Institut National de la Transfusion Sanguine (INTS)
- Agence Nationale de la Recherche (ANR)
- Region Ile-de-France (SESAME program)
- Ministere de l'Enseignement Superieur et de la Recherche
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Migration of circulating leukocytes from the vasculature into the surrounding tissue is an important component of the inflammatory response. Among the cell surface molecules identified as contributing to leukocyte extravasation is VCAM-1, expressed on activated vascular endothelium, which participates in all stages of leukocyte-endothelial interaction by binding to leukocyte surface expressed integrin VLA-4. However, not all VLA-4-mediated events can be linked to VCAM-1. A novel interaction between VLA-4 and endothelial Lutheran (Lu) blood group antigens and basal cell adhesion molecule (BCAM) proteins has been recently shown, suggesting that Lu/BCAM may have a role in leukocyte recruitments in inflamed tissues. Here, we assessed the participation of Lu/BCAM in the immunopathogenesis of crescentic glomerulonephritis. High expression of Lu/BCAM in glomeruli of mice with rapidly progressive glomerulonephritis suggests a potential role for the local expression of Lu/BCAM in nephritogenic recruitment of leukocytes. Genetic deficiency of Lu/BCAM attenuated glomerular accumulation of T cells and macrophages, crescent formation, and proteinuria, correlating with reduced fibrin and platelet deposition in glomeruli. Furthermore, we found a pro-adhesive interaction between human monocyte alpha 4 beta 1 integrin and Lu/BCAM proteins. Thus, Lu/BCAM may have a critical role in facilitating the accumulation of monocytes and macrophages, thereby exacerbating renal injury.
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