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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 70 (1992), S. 89-98 
    ISSN: 1432-1440
    Keywords: Endothelial heterogeneity ; Vascular disorders ; Bacillary angiomatosis/peliosis ; Kaposi's sarcoma ; Acquired immunodeficiency syndrome (AIDS)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Vascular disorders comprise a wide range of diverse disease entities. Correspondingly, vessels, and even more so the endothelia which line them, show a remarkable extent of heterogeneous differentiation, e.g. between the blood vascular and lymphatic systems, along the length of the vascular trees, and in the microvascular beds of various organs. The most important morphologic criterion to discriminate between endothelia is continuity (continuous endothelial cell layer and well-formed basement membrane) versus discontinuity (intra- or intercellular gaps and/or reduced or missing basement membrane). Most blood vascular endothelia are of the continuous type, while most sinusoidal and lymphatic endothelia are discontinuous by these criteria. Antigen expression corroborates these morphologic data in that CD31, CD34, and 11710 antigen are exclusively expressed in continuous endothelia, while MS-1 antigen is preferentially expressed in non-continuous sinusoidal endothelia. In contrast, no specific marker has as yet been described for lymphatic endothelia. Endothelial heterogeneity substantially contributes to the pathogenesis of vascular disorders. For example, in patients with acquired immunodeficiency syndrome the same infectious agent may cause either bacillary angiomatosis (a lobular capillary proliferation) or peliosis (sinusoidal dilatation, endothelial denudation, and development of blood-filled cysts) depending on whether the affected organs have predominantly continuous endothelia or noncontinuous sinusoidal endothelia. Moreover, in Kaposi's sarcoma, it is still an open question of whether the lesion is derived from blood vascular or lymphatic endothelia (Kaposi's sarcoma cells in situ do not express the von Willebrand factor+, PAL-E+, 11710+ phenotype of mature, resting blood vascular endothelia). It is also unresolved how endothelia of either type may be differentially induced to dedifferentiate and how they are recruited into the lesion. Clearly, knowledge about endothelial heterogeneity is still too incomplete to identify the actual mechanisms and molecules that govern the pathogenesis of vascular disorders (including still others than those mentioned here such as atherosclerosis, diabetic angiopathy, and rheumatoid arthritis) affecting distinct endothelia. Further efforts in antigenic phenotyping and in cell and molecular biology of heterogeneously differentiated endothelia should be made to improve this state of affairs.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-069X
    Keywords: Key words Psoriasis ; Mononuclear phagocytes ; Alternatively activated macrophages ; MS-1 high ; molecular weight protein ; RM 3/1 antigen
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Immunological mechanisms play an important role in the pathogenesis of psoriasis. Lesional psoriatic skin-derived T-cell clones have been shown to stimulate keratinocyte proliferation and to predominantly express a T-helper type 1 cytokine pattern. However, T-helper type 2-like cytokines have also been identified in some psoriatic T-cell clones. In parallel to the T-helper type 1/type 2 dichotomy, a distinction between interferon-γ-induced (classically activated) macrophages and interleukin-4/glucocorticoid-induced (alternatively activated) macrophages has been put forward as a conceptual framework for a better understanding of immunopathological processes. In the present study, the phenotype of mononuclear phagocytes in psoriatic skin lesions ( n = 21), allergic contact dermatitis ( n = 4) and normal skin ( n = 2) was investigated using a panel of monoclonal antibodies (mAb) against monocytes/macrophages and dendritic cells (mAb MS-1, RM 3/1, and 25F9 against subsets of in vitro alternatively activated macrophages, and mAb against myeloid antigens CD1a, CD11b, CD11c, CD34, CD36, and CD68). With regard to mononuclear phagocytes, psoriatic skin was found to be compartmentalized into epidermis, subepidermal space, and upper and lower dermis. RM 3/1 +++ , MS-1 ± , 25F9 – dendritic macrophages previously classified as type II alternatively activated macrophages were the dominant dermal macrophage population in psoriatic skin, while intraepidermal and epithelium-lining macrophages expressed a different, presumably classically activated, macrophage phenotype (RM 3/1 – , MS-1 – , 25F9 – , CD68 ++ , CD11b ++ ). In allergic contact dermatitis, a classical T-helper type 1 disease, RM 3/1 +++ macrophages were less prominent. Since MS-1 high molecular weight protein is much more sensitive to interferon-γ-induced suppression than RM 3/1 antigen, a predominance of T-helper type 1 cytokines in psoriasis could explain why dermal dendritic macrophages do not express the fully induced MS-1 +++ , RM 3/1 +++ , 25F9 ± phenotype of type I alternatively activated macrophages.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1173
    Keywords: Schlüsselwörter Akroangiodermatitis ; Morbus Mali ; Stewart-Bluefarb-Syndrom ; Pseudo-Kaposi-Sarkom ; Kaposi-Sarkom ; Key words Acroangiodermatitis ; Morbus Mali ; Stewart-Bluefarb-syndrome ; Pseudo-Kaposi’s-sarcoma ; Kaposi’s sarcoma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary A 76-year-old female patient developed severe manifestations of a kaposi-like acroangiodermatitis (so-called Mali’s disease) due to chronic venous insufficiency of the lower extremities. The patient presented with large areas of confluent, violaceous or brown-black papules on both lower legs. Histologically, proliferation of thick-walled capillaries was seen in the upper dermis consisting of fully differentiated endothelial cells, as shown by immunohistochemistry. In contrast to true Kaposi’s sarcoma, human-herpes-virus-8 DNA could not be detected by polymerase-chain-reaction in this condition. We review the diagnostic criteria used to distinguish between acroangiodermatitis, also called pseudo-Kaposi’s sarcoma, and the true Kaposi’s sarcoma.
    Notes: Zusammenfassung Wir berichten über eine 76jährige Patientin mit einer ausgeprägten kaposiformen Akroangiodermatitis (Morbus Mali), die sich klinisch mit großflächig konfluierenden, lividroten bis bläulich-schwarzen Papeln an beiden Unterschenkeln manifestierte und auf einer chronisch-venösen Insuffizienz Grad II nach Widmer mit Stammvarikosis Grad IV nach Hach sowie Parva- und Perforansinsuffizienzen bereits beruhte. Histologisch fanden sich, beschränkt auf die obere Dermis, prominente, dickwandige Kapillarproliferate, deren Endothelzellen immunhistologisch als ausgereift identifiziert werden konnten. In der Polymerase-Ketten-Reaktion war das Humane Herpes-Virus-8, das neuerdings beim klassischen und HIV-assoziierten, echten Kaposi-Sarkom nachgewiesen wurde, nicht nachweisbar. Das Krankheitsbild war bei unserer Patientin so ausgeprägt, daß wir hier unter Berücksichtigung der neueren Literatur erneut auf die Kriterien zur Abgrenzung der kaposiformen Akroangiodermatitis vom Kaposi-Sarkom eingehen.
    Type of Medium: Electronic Resource
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