References of "Debrus, S"
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See detailDetection of Cytokines in Human Sural Nerve Biopsies: An Immunohistochemical and Molecular Study
Deprez, Manuel ULg; Lübke, U.; Verlaet, Myriam ULg et al

in Acta Neuropathologica (2001), 101(4), 393-404

In vitro and in vivo models have implicated numerous cytokines as major modulators of inflammation, destruction and repair in the peripheral nervous system (PNS). The in situ production of cytokines in ... [more ▼]

In vitro and in vivo models have implicated numerous cytokines as major modulators of inflammation, destruction and repair in the peripheral nervous system (PNS). The in situ production of cytokines in human peripheral nerve disorders is still poorly documented. We studied the expression of interleukin (IL)-1 beta, tumor necrosis factor (TNF)-alpha, IL-6, IL-10, IL-4, IL-3 and nerve growth factor (NGF) in 35 human sural nerve biopsies using immunohistochemistry; additional reverse transcription-polymerase chain reaction and mRNA in situ hybridization were performed for IL-4 and NGF. Expression of IL-1 beta and TNF-alpha was shown in both morphologically normal nerves and various neuropathies, and macrophages appeared as their predominant source. Levels of IL-1 beta and TNF-alpha expression were significantly correlated (P < 0.01) with each other and with expression of NGF. Multiple endoneurial sources were suggested for IL-6 and IL-10 with low immunoreactivity in the vast majority of cases. Conversely, IL-4 and IL-3 expression were found in neuropathies of various etiologies and Schwann cells appeared to be a predominant source of IL-4 in double-labeling immunofluorescence studies. IL-3 immunoreactivity correlated with IL-1 beta, TNF-alpha and IL-6. In this retrospective study, no specific cytokine profile of expression could be assigned to a precise subgroup of neuropathies. This is the first report of IL-4 and IL-3 expression in human neuropathies, and it may be important given the potential role of these cytokines in modulating macrophage activity in the PNS. [less ▲]

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See detailMice Transgenic for a Soluble Form of Murine Cytotoxic T Lymphocyte Antigen 4 Are Refractory to Murine Acquired Immune Deficiency Sydrome Development
de Leval, Laurence ULg; Debrus, S.; Lane, P. et al

in Immunology (1999), 98(4), 630-8

Interactions between B and CD4+ T cells are central to the pathogenesis of retrovirus-induced murine acquired immune deficiency virus (MAIDS). Prompted by previous work showing that treatment with ... [more ▼]

Interactions between B and CD4+ T cells are central to the pathogenesis of retrovirus-induced murine acquired immune deficiency virus (MAIDS). Prompted by previous work showing that treatment with cytotoxic T lymphocyte antigen 4 immunoglobulin (CTLA4Ig) partly inhibited the disease, we studied the course of infection in mice deficient for CD28-B7 interactions (mCTLA4-Hgamma1 transgenic mice). Despite a relative viral load identical to that of non-transgenic mice, the transgenic mice did not develop any of the major MAIDS symptoms (i.e. lymphoproliferation and immune anergy). The mCTLA4-Hgamma1 did not however, completely inhibit B-cell activation as indicated by a slight hypergammaglobulinaemia and microscopic blastic transformation. Absence of MAIDS in transgenic mice was associated with much lower levels of both interleukin-4 and interferon-gamma transcripts following viral infection. These results support the theory that the CD28/B7 costimulatory pathway is a critical determinant to MAIDS development. [less ▲]

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See detailCd28-B7 Costimulatory Blockade by Ctla4ig Delays the Development of Retrovirus-Induced Murine Aids
de Leval, Laurence ULg; Colombi, S.; Debrus, S. et al

in Journal of Virology (1998), 72(6), 5285-90

Mouse AIDS (MAIDS) induced in C57BL/6 mice by infection with a replication-defective retrovirus (Du5H) combines extensive lymphoproliferation and profound immunodeficiency. Although B cells are the main ... [more ▼]

Mouse AIDS (MAIDS) induced in C57BL/6 mice by infection with a replication-defective retrovirus (Du5H) combines extensive lymphoproliferation and profound immunodeficiency. Although B cells are the main target of viral infection, recent research has focused on CD4(+) T cells, the activation of which is a key event in MAIDS induction and progression. A preliminary observation of increased expression of B7 molecules on B cells in MAIDS prompted us to address the possible involvement of the CD28/B7 costimulatory pathway in MAIDS. Mice infected with the MAIDS-inducing viral preparation were treated with murine fusion protein CTLA4Ig (3 x 50 microg/week given intraperitoneally), a competitive inhibitor of physiological CD28-B7 interactions. In CTLA4Ig-treated animals, the onset of the disease was delayed, lymphoproliferation progressed at a much slower rate than in untreated mice, and the loss of in vitro responsiveness to mitogens was reduced. Relative expression of Du5H did not differ between treated and untreated animals. These results suggest that the CD28/B7 costimulatory pathway contributes to MAIDS development. [less ▲]

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See detailDistribution of varicella-zoster virus gpI and gpII and corresponding genome sequences in the skin
Nikkels, Arjen ULg; Delvenne, Philippe ULg; Debrus, S. et al

in Journal of Medical Virology (1995), 46(2), 91-96

In the course of varicella-zoster virus (VZV) infection, some viral capsid antigens are found in the epidermis and dermis. The aim of this study was to investigate the localisation of two major VZV ... [more ▼]

In the course of varicella-zoster virus (VZV) infection, some viral capsid antigens are found in the epidermis and dermis. The aim of this study was to investigate the localisation of two major VZV glycoproteins (gpI and gpII) and of their respective genes in the skin. The distribution of VZV gpI and II in 27 formalin fixed paraffin embedded skin biopsies from herpes tester eruptions were compared by immunohistochemistry. Double immunostaining was carried our to identify infected cells. The presence of viral nucleic acids coding for gpI and gpII was examined by in situ hybridisation. The distribution of gpI and gpII and their corresponding genome sequences was similar in the epidermis, gpI and gpII were also detected in dermal FXIIIa positive dendrocytes, in Mac 387 and CD68 positive macrophages, and in perineural and endothelial cells. However, the corresponding viral nucleic acids were rarely and barely detected in these cells of the dermis. It is concluded that VZV infection of epithelial cells follows a different course than in dermal cells. (C) 1995 Wiley-Liss, Inc. [less ▲]

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See detailExpression of several viral proteins during the varicella-zoster virus infectious cycle
Debrus, S.; Kinchington, P. R.; Piette, Jacques ULg et al

Conference (1995)

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See detailLocalization of varicella-zoster virus nucleic acids and proteins in human skin.
Nikkels, Arjen ULg; Debrus, S.; Sadzot-Delvaux, Catherine ULg et al

in Neurology (1995), 45(12 Suppl 8), 47-9

The pathogenic mechanisms involved in varicella-zoster virus (VZV) infections remain elusive. The pattern of cutaneous distribution of the IE63 protein and of the gpI (gE) and gpII glycoproteins with ... [more ▼]

The pathogenic mechanisms involved in varicella-zoster virus (VZV) infections remain elusive. The pattern of cutaneous distribution of the IE63 protein and of the gpI (gE) and gpII glycoproteins with their corresponding genome sequences during VZV infections was studied by immunohistochemistry and in situ hybridization. Skin biopsy specimens were obtained from immunocompetent and immunocompromised patients with varicella, herpes zoster, or atypical VZV lesions. The first evidence for VZV infection consisted of the presence of IE63 in keratinocytes. In the vesicles and pustules, the viral transcripts gpI, gpII, and IE63 and the corresponding nucleic acids for gpI and gpII were identified in keratinocytes, sebocytes, Langerhans cells, dermal dendrocytes, monocytes/macrophages, and endothelial cells. The gpI and gpII glycorpoteins were essentially located on the cellular membranes while IE63 expression was generally restricted to the nuclei. In three biopsies of early herpes zoster, viral proteins were disclosed in dermal nerves and in perineurial type I dendrocytes. This was never encountered in varicella. Vasculitic changes and endothelial cell involvement were more prominent in varicella than in herpes zoster. It is concluded that the secondary viremia in varicella that affects the dermal endothelial cells is followed by a cell-to-cell spread to keratinocytes. In herpes zoster, the viral progression through cutaneous nerves primarily extends to the pilosebaceous units with a secondary involvement of epidermal keratinocytes, followed by a further spread to dermal cells. [less ▲]

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See detailImmunohistochemical identification of varicella-zoster virus gene 63-encoded protein (IE63) and late (gE) protein on smears and cutaneous biopsies: implications for diagnostic use.
Nikkels, Arjen ULg; Debrus, S.; Sadzot-Delvaux, Catherine ULg et al

in Journal of Medical Virology (1995), 47(4), 342-7

Early and specific recognition of varicella zoster virus (VZV) infection is of vital concern in immunocompromised patients. The aim of this study was to compare the diagnostic accuracy of histochemical ... [more ▼]

Early and specific recognition of varicella zoster virus (VZV) infection is of vital concern in immunocompromised patients. The aim of this study was to compare the diagnostic accuracy of histochemical and immunohistochemical identification of the VZV ORF63 encoded protein (IE63) and of the VZV late protein gE on smears and formalin-fixed paraffin-embedded skin sections taken from lesions clinically diagnosed as varicella (n = 15) and herpes zoster (n = 51). Microscopic examinations of Tzanck smears and skin sections yielded a diagnostic accuracy of Herpesviridae infections in 66.7% (10/15) and 92.3% (12/13) of varicella, and 74.4% (29/39) and 87.8% (43/49) of herpes zoster, respectively. Immunohistochemistry applied to varicella provided a type-specific virus diagnostic accuracy of 86.7% (13/15; IE63) and 100% (15/15; gE) on smears, and of 92.3% for both VZV proteins on skin sections. In herpes zoster, the diagnostic accuracy of immunohistochemistry reached 92.3% (36/39; IE63) and 94.9% (37/39; gE) on smears, and 91.7% (44/48; IE63) and 91.8% (45/49; gE) on skin sections. These findings indicate that the immunohistochemical detection of IE63 and gE on both smears and skin sections yields a higher specificity and sensitivity than standard microscopic assessments. [less ▲]

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See detailViral glycoproteins in herpesviridae granulomas
Nikkels, Arjen ULg; Debrus, S.; Delvenne, Philippe ULg et al

in American Journal of Dermatopathology (1994), 16(6), 588-592

Granulomatous reactions after varicella zoster virus (VZV) and herpes simplex virus (HSV) infections are rare, and their pathogenesis remains unclear. We studied by immunohistochemistry and in situ ... [more ▼]

Granulomatous reactions after varicella zoster virus (VZV) and herpes simplex virus (HSV) infections are rare, and their pathogenesis remains unclear. We studied by immunohistochemistry and in situ hybridization early granulomatous reactions after VZV and HSV infections. In the five cases studied, the VZV glycoproteins gp I and gp II were present in cells abutted to altered vessels, but the corresponding genome sequences were disclosed in similar locations in only one of these cases. In an immunocompromised patient with diffuse HSV eruption, HSV I antigens were present in cells of the reticular dermis, while viral nucleic acids were not evident. Immunophenotyping of the granulomas showed strong Mac 387 and CD68 positive labelings of macrophages/monocytes, without any involvement of Factor XIIIa-positive cells. These findings suggest that the major viral envelope glycoproteins, rather than complete viral particles could trigger granuloma formation following HSV and VZV skin infections. [less ▲]

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See detailCausative role of VZV in two fatal disseminated infections
Nikkels, Arjen ULg; Debrus, S.; Sadzot-Delvaux, Catherine ULg et al

Conference (1994)

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See detailCharacterization of an in vivo model of VZV latency in the nervous system
Sadzot-Delvaux, Catherine ULg; Nikkels, Arjen ULg; Debrus, S. et al

Conference (1994)

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See detailImmunohistochemical detection of immediate early and late phase proteins expressed during the varicella-zoster virus cycle
Nikkels, Arjen ULg; Debrus, S.; Sadzot-Delvaux, Catherine ULg et al

in British Journal of Dermatology. Supplement (1994), 131(44), 64

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See detailComparative immunohistochemical study of herpes-simplex and varicella-zoster infections
Nikkels, Arjen ULg; Debrus, S.; Sadzot-Delvaux, Catherine ULg et al

in Virchows Archiv. A : Pathological Anatomy and Histopathology (1993), 422(2), 121-126

Herpes simplex (HSV) and varicella-zoster (VZV) skin infections share so many histological similarities that distinguishing between them may prove to be impossible. We developed and characterized a new ... [more ▼]

Herpes simplex (HSV) and varicella-zoster (VZV) skin infections share so many histological similarities that distinguishing between them may prove to be impossible. We developed and characterized a new monoclonal antibody, VL8, IgG kappa isotype, directed to the VZV envelope glycoprotein gpI. Immunohistochemistry with VL8 appeared highly sensitive and specific on formalin-fixed paraffin-embedded biopsies and a clear-cut distinction between HSV and VZV infections was possible. The pattern of VL8 immunolabelling in VZV infections was strikingly different from that found in HSV infections studied with polyclonal antibodies to HSV I and II. Double immunolabelling revealed the VL8 positivity of sebaceous cells, endothelial cells, Mac 387-and CD68-positive monocyte-macrophages, and factor XIIIa-positive perivascular, perineural and interstitial dendrocytes. Intracytoplasmic VL8 labelling of endothelial cells and perivascular dendrocytes was found at the site of leukocytoclastic vasculitis. [less ▲]

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See detailLa régulation de l'expression des gènes du virus de la varicelle et du zona
Piette, Jacques ULg; Defechereux, Patricia; Baudoux, Laurence et al

in Annales de Médecine Vétérinaire (1992), 136(8), 627-635

Varicella-zoster virus (VZV) belongs to the alphaherpesvirus family and shares many important structural and functional similarities with other members of the family such as herpes simplex virus type 1 ... [more ▼]

Varicella-zoster virus (VZV) belongs to the alphaherpesvirus family and shares many important structural and functional similarities with other members of the family such as herpes simplex virus type 1 (HSV-1). VZV is responsible for two different clinical syndromes, varicella which is the result of the primary infection and zoster which is due to virus reactivation remaining latent in the peripheral nervous system. VZV DNA is 124,884 base pair long and encodes four regulatory proteins (IE4, IE61, IE62 and IE63). Using transient expression systems, we have shown that IE4, IE62 and IE63 can regulate the expression of an indicator gene driven by various VZV promoter regions, demonstrating that these proteins play important roles in the infectious cycle. [less ▲]

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See detailTwo-dimensional study of varicella-zoster virus proteins
Debrus, S.; Duquesne, Patricia ULg; Sadzot-Delvaux, Catherine ULg et al

Poster (1992)

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See detailTwo-dimensional study of varicella-zoster virus proteins
Debrus, S.; Lebon, L.; Schoonbroodt, Sonia et al

in Archives Internationales de Physiologie, de Biochimie et de Biophysique (1992), 100(2), 39

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See detailVZV glycoproteins gpI and gpII are present in dermal cells without their corresponding genome
Nikkels, Arjen ULg; Delvenne, Philippe ULg; Debrus, S. et al

in Journal of Cutaneous Pathology (1992), 19

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