Erythrophagocytosis in Kaposi’s Sarcoma in Acquired Immune Deficiency Syndrome

Schenk, Peter

doi:10.1159/000275863

Cited by 6 publications

(8 citation statements)

References 17 publications

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“…Prior work has shown macrophage involvement in cerebral microbleeds (4,6). Pericytes are also known to have phagocytic function (14, 20) and erythrophagocytosis has been observed in systemic pericytes (21, 22). …”

Section: Discussionmentioning

confidence: 99%

Cerebral Microbleeds in the Elderly

Fisher

French

et al. 2010

Stroke

154

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Background and Purpose-Cerebral microbleeds in the elderly are routinely identified by brain MRI. The purpose of this study was to better characterize the pathological basis of microbleeds. Methods-We studied postmortem brain specimens of 33 individuals with no clinical history of stroke and with an age range of 71 to 105 years. Cerebral microbleeds were identified by presence of hemosiderin (iron), identified by routine histochemistry and Prussian blue stain. Cellular localization of iron (in macrophages and pericytes) was studied by immunohistochemistry for smooth muscle actin, CD68, and, in selected cases, electron microscopy. Presence of ␤-amyloid was analyzed using immunohistochemistry for epitope 6E10. Results-Cerebral microbleeds were present in 22 cases and occurred at capillary, small artery, and arteriolar levels.Presence of microbleeds occurred independent of amyloid deposition at site of microbleeds. Although most subjects had hypertension, microbleeds were present with and without hypertension. Putamen was the site of microbleeds in all but 1 case; 1 microbleed was in subcortical white matter of occipital lobe. Most capillary microbleeds involved macrophages, but the 2 microbleeds studied by electron microscopy demonstrated pericyte involvement. Key Words: amyloid angiopathy Ⅲ blood-brain barrier Ⅲ hemorrhage, intracerebral Ⅲ hemosiderin Ⅲ hypertension Ⅲ phagocytosis I ncreasing reliance on MRI of stroke patients has emphasized substantial prevalence and significance of cerebral microbleeds in the aging population. MRI using state-of-theart gradient-echo sequences has demonstrated cerebral microbleeds in 18% of individuals between ages 60 to 69 years and in 38% of individuals older than age 80. 1 Moreover, presence of cerebral microbleeds appears to increase risk of warfarin-associated intracerebral hemorrhage Ͼ80-fold, 2 and use of platelet aggregation inhibitors is associated with presence of microbleeds. 3 These findings underscore the importance of cerebral microbleeds. Conclusions-TheseDespite their importance, cerebral microbleeds have received only limited attention in pathological analyses. Recent work has examined in detail cerebral microbleeds in cerebral amyloid angiopathy, 4 demonstrating strong correlation between microbleeds in postmortem brain tissue and MRI lesions. The consensus view is that microbleeds of lobar location reflect underlying cerebral amyloid angiopathy, whereas deep subcortical microbleeds indicate hypertensive vasculopathy. 1,[5][6][7][8] The purpose of the present study was to expand our knowledge of the pathology of cerebral microbleeds in the aging brain. Our focus was the vascular abnormalities underlying cerebral microbleeds, including vessel type, presence of associated amyloid angiopathy, and range of cellular involvement in the microbleeds themselves. Materials and MethodsThe investigation consisted of 2 studies of brain tissue from elderly subjects. Initial survey study consisted of 12 subjects who underwent autopsy between January 2006 and December 2008 wit...

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Section: Discussionmentioning

confidence: 99%

Cerebral Microbleeds in the Elderly

Fisher

French

et al. 2010

Stroke

154

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“…It participates in the phagocytic process, and in the clearance of (36). The receptor for the C3d fragment of C3 (CR2) has been shown to be the Epstein-Barr virus receptor (16,37).…”

Section: Methodsmentioning

confidence: 99%

Expression and localization of proteins of the complement system in human skin.

Dovezenski¹,

Billetta²,

Gigli³

1992

J. Clin. Invest.

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The complement system participates in the immune recognition of foreign antigens, many of which may penetrate the skin by physical injury or transcutaneous adsorption. In this study, we examined the presence of complement components and complement regulatory proteins in the human skin and cultured human keratinocytes. Immunofluorescence studies showed C3, Factor B, decay accelerating factor, the C3b receptor (CR1), and C3d receptor (CR2), distributed among cells of the epidermis as well as on cultured keratinocytes. Immunoblot analysis of keratinocytes supernatants showed the presence ofC3 with a molecular weight of 180 kD. The decay accelerating factor was localized as previously reported on elastic fibers; additionally it was observed in the basement membrane zone. In situ hybridization studies suggest the expression of CR1 and CR2 mRNA in human epidermis. These results show the presence in the human epidermis of complement components that are capable of generating the initial C3 convertase of the alternative pathway. The presence of complement regulatory proteins could endow keratinocytes with immune functions such as the regulation of complement activation and endocytosis of C3 opsonized parti-

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“…The location of the pericyte opposite the inter-endothelial junction in effect constitutes a “gate” preventing egress of blood constituents (Fig 3). This gatekeeper element of the pericyte, preventing exit of erythrocytes, may then be amplified by the erythrophagocytic function that is well-described in systemic pericytes (25,26). …”

Section: Characteristics Of Brain-specific Regulationmentioning

confidence: 99%

Brain Regulation of Thrombosis and Hemostasis

Fisher

2013

Stroke

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Erythrophagocytosis in Kaposi’s Sarcoma in Acquired Immune Deficiency Syndrome

Cited by 6 publications

References 17 publications

Cerebral Microbleeds in the Elderly

Cerebral Microbleeds in the Elderly

Expression and localization of proteins of the complement system in human skin.

Brain Regulation of Thrombosis and Hemostasis

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