Base de dados : HANSEN Pesquisa : REGULACAO PARA CIMA [Descritor de assunto] Referências encontradas : 2 [refinar] Mostrando: 1 .. 2   no formato [Detalhado]

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Id: 18575 Autor: Cheadle, Eleanor J; Selby, Peter J; Jackson, Andrew M Título: Mycobacterium bovis bacillus Calmette-Guérin-infected dendritic cells potently activate autologous T cells via a B7 and interleukin-12-dependent mechanism ..- Fonte: s.l; s.n; 2003. 10 p. graf. Resumo: Mycobacteria are potent adjuvants, can survive intracellularly and have been safely used for many years as vaccines against tuberculosis and leprosy. They are thus important potential vectors for recombinant vaccines. Many of their adjuvant properties are mediated following phagocytosis by dendritic cells (DC), which are in turn critical for priming naïve T cells. Although the maturation of DC in response to mycobacteria, such as Mycobacterium bovis bacillus Calmette-Guérin (BCG), is well described the subsequent responses of autologous T cells to mycobacterium-infected DC remains uncharacterized. In our experiments DC infected with BCG expressed more co-stimulatory molecules than tumour-necrosis factor-alpha (TNF-alpha) -treated DC and stimulated more potent mixed leucocyte reactions. When autologous T cells were co-cultured with BCG-exposed DC they became highly activated, as determined by display of CD25, CD54 and CD71 on both CD4+ and CD8+ cells. In contrast, the response of T cells to TNF-alpha-matured DC was significantly less. Cytokine production from T cells cultured with BCG-exposed DC was enhanced with elevated secretion of interleukin-2 (IL-2), IL-10 and interferon-gamma (IFN-gamma) and was produced by both CD4+ and CD8+ lymphocytes as determined by intracellular staining. In particular, IFN-gamma secretion was increased from 50 pg/ml to 25 000 pg/ml and IL-10 secretion increased from 20 pg/ml to 300 pg/ml in BCG-exposed DC co-cultures. Blocking antibodies to B7.1 and B7.2 or IL-12 significantly reduced the secretion of IFN-gamma and reductions were also seen in the expression of CD25 and CD71 by CD4+ cells. These data demonstrate that mycobacterially infected DC are particularly potent activators of autologous T cells compared to TNF-alpha-exposed DC and that the resultant T cells are functionally superior. (AU). Descritores: ANTIGENOS CD/metab ANTIGENOS CD80/imunol ANTIGENOS DE DIFERENCIACAO DE LINFOCITOS B/metab LINFOCITOS T CD4-POSITIVOS/imunol LINFOCITOS T CD8-POSITIVOS/imunol CITOCINAS/bios CELULAS DENDRITICAS/imunol CELULAS DENDRITICAS/microbiol MOLECULA 1 DE ADESAO INTERCELULAR IMUNOFENOTIPAGEM INTERLEUCINA-12/imunol TRANSFORMACAO LINFOCITICA/imunol MYCOBACTERIUM BOVIS/imunol RECEPTORES DA INTERLEUCINA-2/metab LINFOCITOS T/imunol FATOR DE NECROSE TUMORAL/imunol REGULACAO PARA CIMA/imunol Limites: HUMANO SUPPORT, NON-U.S. GOV'T Meio Eletrônico: - . Localização: BR191.1; 08996/s

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Id: 18504 Autor: Bleharski, Joshua R; Li, Huiying; Meinken, Christoph; Graeber, Thomas G; Ochoa, Maria-Teresa; Yamamura, Masahiro; Burdick, Anne; Sarno, Euzenir N; Wagner, Manfred; Röllinghoff, Martin; Rea, Thomas H; Colonna, Marco; Stenger, Steffen; Bloom, Barry R; Eisenberg, David; Modlin, Robert L Título: Use of genetic profiling in leprosy to discriminate clinical forms of the disease ..- Fonte: s.l; s.n; Sep. 2003. 4 p. graf. Resumo: Leprosy presents as a clinical and immunological spectrum of disease. With the use of gene expression profiling, we observed that a distinction in gene expression correlates with and accurately classifies the clinical form of the disease. Genes belonging to the leukocyte immunoglobulin-like receptor (LIR) family were significantly up-regulated in lesions of lepromatous patients suffering from the disseminated form of the infection. In functional studies, LIR-7 suppressed innate host defense mechanisms by shifting monocyte production from interleukin-12 toward interleukin-10 and by blocking antimicrobial activity triggered by Toll-like receptors. Gene expression profiles may be useful in defining clinical forms of disease and providing insights into the regulation of immune responses to pathogens. (AU). Descritores: HANSENIASE VIRCHOWIANA/clas HANSENIASE VIRCHOWIANA/genet HANSENIASE VIRCHOWIANA/imunol HANSENIASE VIRCHOWIANA/fisiopatol HANSENIASE TUBERCULOIDE/clas HANSENIASE TUBERCULOIDE/genet HANSENIASE TUBERCULOIDE/imunol HANSENIASE TUBERCULOIDE/fisiopatol CITOCINAS/genet CITOCINAS/metab PERFILACAO DA EXPRESSÃO GÊNICA ANALISE POR CONGLOMERADOS CONTAGEM DE COLÔNIA MICROBIANA REGULACAO DA EXPRESSÃO GÊNICA IMUNIDADE CELULAR IMUNIDADE NATURAL MACROFAGOS ALVEOLARES/microbiol GLICOPROTEINAS DE MEMBRANA/imunol MYCOBACTERIUM TUBERCULOSIS/cresc MYCOBACTERIUM TUBERCULOSIS/imunol REACAO EM CADEIA DA POLIMERASE RECEPTORES IMUNOLOGICOS/genet RECEPTORES IMUNOLOGICOS/metab RECEPTORES DA SUPERFICIE CELULAR/imunol - REGULACAO PARA CIMA  Análise de Componente Principal  ALGORITMOS  GENES DE IMUNOGLOBULINAS  ANALISE DE SEQUÊNCIA COM SERIES DE OLIGONUCLEOTIDIOS Limites: SUPPORT, NON-U.S. GOV'T HUMANO SUPPORT, U.S. GOV'T, P.H.S. Meio Eletrônico: - . Localização: BR191.1; 09142/s; BR191.1; 09145/s

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