In situ labelling of fragmented DNA in cutaneous necrotizing vasculitis

Barduagni, S; Frezzolini, Alessandra; Ferranti, G; Papi, Massimo; Pità, Ornella De

doi:10.1016/s0923-1811(98)00007-3

Cited by 2 publications

(2 citation statements)

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“…Recent studies on the nature of the neutrophilic infiltrate showed a strong positive staining with in situ nick end labeling techniques, thereby demonstrating DNA breakdown in the infiltrating neutrophils. In these lesions, only a minor part is typically apoptotic, whereas the majority of neutrophils shows breakdown of DNA with disintegrated cytoplasmic organelles and plasma membrane 42,43. The phenomenon of leukocytoclasia is interesting since normally dying cells are quickly engulfed by phagocytes, particularly at sites of inflammation.…”

Section: Disturbances In the Clearance Of Neutrophilsmentioning

confidence: 99%

“…In these lesions, only a minor part is typically apoptotic, whereas the majority of neutrophils shows breakdown of DNA with disintegrated cytoplasmic organelles and plasma membrane. 42,43 The phenomenon of leukocytoclasia is interesting since normally dying cells are quickly engulfed by phagocytes, particularly at sites of inflammation. Furthermore, the accumulation of dying cells and the presence of nuclear debris in these lesions suggest that the removal of apoptotic or necrotic cells is incomplete.…”

Section: Disturbances In the Clearance Of Neutrophilsmentioning

confidence: 99%

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Activation, Apoptosis, and Clearance of Neutrophils in Wegener's Granulomatosis

Rossum

Limburg

Kallenberg

2005

Annals of the New York Academy of Sciences

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Wegener's granulomatosis (WG) is strongly associated with the presence of antineutrophil cytoplasmic autoantibodies (ANCAs). Within WG these ANCAs are usually (80-90%) directed against the azurophilic enzyme proteinase 3, the so called PR3-ANCA. A pathophysiological role for these autoantibodies, supported by numerous in vitro and in vivo studies, is specifically based on their capacity to bind and activate neutrophils and potentially may damage vessels. In this review, the pathogenic potential of different developmental stages of the neutrophil in the pathogenesis of WG is discussed. After release from the bone marrow into the circulation, neutrophils can be primed by TNFalpha and become attached to locally activated endothelium. Once attached to the endothelium, ANCAs can fully activate these primed neutrophils. In this activation process, the degree of activation after stimulation with PR3-ANCAs associates with the level of PR3 expression on the membrane of the neutrophil. Following activation, infiltrated neutrophils become apoptotic with further membrane expression of PR3. In WG patients, clearance of apoptotic neutrophils can be disturbed due to the opsonization of PR3-expressing apoptotic neutrophils with PR3-ANCAs, thereby perpetuating inflammation by the release of proinflammatory cytokines during clearance; or it may favor autoimmunity by PR3 presentation in an inflammatory environment. Furthermore, the presence of ANCAs and the release of the vessel-related pentraxin PTX3 may lead to the persistence of late apoptotic neutrophils in tissues, thereby inducing leukocytoclastic lesions that are characteristic in patients with WG. All together, alive neutrophils as well as apoptotic neutrophils play a key role in different inflammatory phenomena seen in patients suffering from WG.

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Section: Disturbances In the Clearance Of Neutrophilsmentioning

confidence: 99%

Section: Disturbances In the Clearance Of Neutrophilsmentioning

confidence: 99%