Endothelium-neutrophil interactions in ANCA-associated diseases

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Quantitative In vitro Assay to Measure Neutrophil Adhesion to Activated Primary Human Microvascular Endothelial Cells under Static Conditions
11:22

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Published on: August 23, 2013

Lise Halbwachs1, Philippe Lesavre

  • 1Institut National de la Santé et de la Recherche Medicale INSERM U845, Université Paris Descartes, Sorbonne Paris Cité, France.

Journal of the American Society of Nephrology : JASN
|September 4, 2012
PubMed

The two salient features of ANCA-associated vasculitis (AAV) are the restricted microvessel localization and the mechanism of inflammatory damage, independent of vascular immune deposits. The microvessel localization of the disease is due to the ANCA antigen accessibility, which is restricted to the membrane of neutrophils engaged in β2-integrin-mediated adhesion, while these antigens are cytoplasmic and inaccessible in resting neutrophils. The inflammatory vascular damage is the consequence of maximal proinflammatory responses of neutrophils, which face cumulative stimulations by TNF-α, β2-integrin engagement, C5a, and ANCA by the FcγRII receptor. This results in the premature intravascular explosive release by adherent neutrophils of all of their available weapons, normally designed to kill IgG-opsonized bacteria after migration in infected tissues.

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