Base de dados : MEDLINE
Pesquisa : B04.280.650.160.550 [Categoria DeCS]
Referências encontradas : 3 [refinar]
Mostrando: 1 .. 3   no formato [Detalhado]

página 1 de 1

  1 / 3 MEDLINE  
              next record last record
para imprimir
Texto completo
[Au] Autor:Molina-Ruiz AM; Bernárdez C; Requena L; Schärer L
[Ad] Endereço:Department of Dermatology, Fundación Jiménez Díaz, Universidad Autónoma, Madrid, Spain.
[Ti] Título:Primitive follicular induction in molluscum contagiosum.
[So] Source:J Cutan Pathol;43(1):12-7, 2016 Jan.
[Is] ISSN:1600-0560
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Molluscum contagiosum (MC) is the commonest human poxvirus infection. Follicular induction has rarely been observed in the epidermis surrounding lesions of MC. A virus-induced localized proliferation of germinative/stem cells of the folliculosebaceous-apocrine unit has been suggested as the underlying cause, however few reports of this peculiar phenomenon exist in the literature and the mechanisms involved in this proliferation require further study. METHODS: We prospectively collected MC cases showing multifocal areas of primitive follicular induction involving the adjacent undersurface epidermis. Immunohistochemical expression of BerEP4, PHLDA1 and cytokeratin 20 (CK20) was evaluated in the basaloid germs surrounding the lesions. For PHLDA1, we used epidermal melanocytes as a positive internal control. For BerEP4, we employed a basal cell carcinoma (BCC) and for CK20, colon as positive external controls. An incubation without the primary antibody functioned as an external negative control. RESULTS: All the cases studied showed an intense positive staining of the basaloid buds with BerEP4 and weaker stain for PHLDA1. CK20 showed the presence of scattered Merkel cells within the induced epidermal basaloid proliferations favoring their reactive origin. DISCUSSION: The pathogenetic mechanisms behind the development of these microscopic features and the link between follicular induction and poxvirus infection are explored. Awareness of this unusual phenomenon by dermatopathologists will be helpful in avoiding a misdiagnosis of a superficial BCC in such cases. CONCLUSIONS: BerEP4 and PHLDA1 were consistently expressed in the areas of primitive follicular induction surrounding lesions of MC. CK 20 stained the Merkel cells present in the basaloid buds. All these findings support the reactive origin of this phenomenon, which we believe is most probably viral-induced.
[Mh] Termos MeSH primário: Folículo Piloso/patologia
Molusco Contagioso/patologia
[Mh] Termos MeSH secundário: Biomarcadores Tumorais/metabolismo
Carcinoma Basocelular/metabolismo
Carcinoma Basocelular/patologia
Estudos de Casos e Controles
Folículo Piloso/metabolismo
Folículo Piloso/virologia
Seres Humanos
Células de Merkel/metabolismo
Células de Merkel/patologia
Células de Merkel/virologia
Molluscipoxvirus/isolamento & purificação
Molusco Contagioso/metabolismo
Molusco Contagioso/virologia
Infecções por Poxviridae/metabolismo
Infecções por Poxviridae/patologia
Infecções por Poxviridae/virologia
Estudos Prospectivos
Neoplasias Cutâneas/metabolismo
Neoplasias Cutâneas/patologia
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Keratin-20); 0 (PHLDA1 protein, human); 0 (Transcription Factors); 0 (human epithelial antigen-125)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150813
[St] Status:MEDLINE
[do] DOI:10.1111/cup.12584

  2 / 3 MEDLINE  
              first record previous record next record last record
para imprimir
[Au] Autor:Thurau M; Everett H; Tapernoux M; Tschopp J; Thome M
[Ad] Endereço:Department of Biochemistry, University of Lausanne, BIL Biomedical Research Center, Chemin des Boveresses 155, Epalinges, Switzerland.
[Ti] Título:The TRAF3-binding site of human molluscipox virus FLIP molecule MC159 is critical for its capacity to inhibit Fas-induced apoptosis.
[So] Source:Cell Death Differ;13(9):1577-85, 2006 Sep.
[Is] ISSN:1350-9047
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Members of the viral Flice/caspase-8 inhibitory protein (v-FLIP) family prevent induction of apoptosis by death receptors through inhibition of the processing and activation of procaspase-8 and -10 at the level of the receptor-associated death-inducing signaling complex (DISC). Here, we have addressed the molecular function of the v-FLIP member MC159 of the human molluscum contagiosum virus. MC159 FLIP powerfully inhibited both caspase-dependent and caspase-independent cell death induced by Fas. The C-terminal region of MC159 bound TNF receptor-associated factor (TRAF)3, was necessary for optimal TRAF2 binding, and mediated the recruitment of both TRAFs into the Fas DISC. TRAF-binding-deficient mutants of MC159 showed impaired inhibition of FasL-induced caspase-8 processing and Fas internalization, and had reduced antiapoptotic activity. Our findings provide evidence that a MC159/TRAF2/TRAF3 complex regulates a new aspect of Fas signaling, and identify MC159 FLIP as a molecule that targets multiple features of Fas-induced cell death.
[Mh] Termos MeSH primário: Apoptose/fisiologia
Proteína Reguladora de Apoptosis Semelhante a CASP8 e FADD/metabolismo
Proteína Ligante Fas/fisiologia
Fator 3 Associado a Receptor de TNF/metabolismo
Proteínas Virais/metabolismo
[Mh] Termos MeSH secundário: Sítios de Ligação
Caspase 10/metabolismo
Caspase 8/metabolismo
Linhagem Celular
Proteína Ligante Fas/farmacologia
Seres Humanos
Células Jurkat
Transdução de Sinais
Fator 2 Associado a Receptor de TNF/metabolismo
[Nm] Nome de substância:
0 (CASP8 and FADD-Like Apoptosis Regulating Protein); 0 (Fas Ligand Protein); 0 (TNF Receptor-Associated Factor 2); 0 (TNF Receptor-Associated Factor 3); 0 (TRAF3 protein, human); 0 (Viral Proteins); EC 3.4.22.- (Caspase 10); EC 3.4.22.- (Caspase 8)
[Em] Mês de entrada:0611
[Cu] Atualização por classe:060814
[Lr] Data última revisão:
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:060118
[St] Status:MEDLINE

  3 / 3 MEDLINE  
              first record previous record
para imprimir
[Au] Autor:Smith KJ; Skelton H
[Ad] Endereço:Department of Dermatology and Pathology, University of Alabama, Birmingham, AL 35294, USA.
[Ti] Título:Molluscum contagiosum: recent advances in pathogenic mechanisms, and new therapies.
[So] Source:Am J Clin Dermatol;3(8):535-45, 2002.
[Is] ISSN:1175-0561
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:Two poxviruses, Molluscum contagiosum virus (MCV) and Variola virus are specific to humans. MCV is present worldwide and is directly passed by direct skin to skin contact to produce cutaneous and, rarely, mucosal lesions. It occurs predominantly in preadolescent children, sexually active adults, participants in sports with skin to skin contact, and in individuals with impaired cellular immunity. MCV characteristically proliferates within the follicular epithelium, and with routine fixation produces an area of retraction artifact separating layers 1 to 3 of CD34+ stromal cells that immediately surround the follicle from the surrounding dermis. This feature may be obscured when the lesions are inflamed, usually after rupture into the surrounding dermis. MCV is a cytoplasmically replicating virus. MCV-infected cells grow in size, while internal organelles are dislocated and eventually obliterated by a large intracytoplasmic inclusion. Rupture and discharge of the virus-packed cells occurs in a process similar to membrane debris and MCV accumulate in the crater-like ostium; MCV infection is spread by contact with infectious debris. In HIV-1-positive patients the histologic features, as well as the clinical features, may be atypical in patients with MCV infections. Not only are the lesions often large, but they may be verrucous and markedly hyperkeratotic. Recent sequencing of the MCV genome has increased our understanding and investigations into its mechanisms for avoiding host defense mechanisms. These include regions which encode for homologues of cellular chemokines and chemokine-binding proteins, a homolog of MHC1 and a viral FLICE-like inhibitory protein. Treatment, until recently, has depended upon tissue destruction including curettage, cryotherapy, CO(2) laser, electrodesiccation, trichloracetic acid and cantharadin. Recently, topical immune modulators have been used with some success. Understanding of the MCV genome is providing the basis for the development of drugs for therapy and prevention of MCV infections.
[Mh] Termos MeSH primário: Molusco Contagioso/patologia
Molusco Contagioso/terapia
[Mh] Termos MeSH secundário: Adjuvantes Imunológicos/uso terapêutico
Antineoplásicos/uso terapêutico
Antivirais/uso terapêutico
Terapia Combinada
DNA Viral/genética
Seres Humanos
Hidróxidos/uso terapêutico
Molusco Contagioso/genética
Compostos de Potássio/uso terapêutico
Nitrato de Prata/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Adjuvants, Immunologic); 0 (Antineoplastic Agents); 0 (Antiviral Agents); 0 (DNA, Viral); 0 (Hydroxides); 0 (Potassium Compounds); 95IT3W8JZE (Silver Nitrate); WZH3C48M4T (potassium hydroxide)
[Em] Mês de entrada:0212
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:021003
[St] Status:MEDLINE

página 1 de 1

Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  

Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde