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10.4049/jimmunol.170.2.1010 http://scihub22266oqcxt.onion/10.4049/jimmunol.170.2.1010 12517968!ä!12517968 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=12517968&cmd=llinks): Failed to open stream: HTTP request failed! 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Autocrine type I IFN and contact with endothelium promote the presentation of influenza A virus by monocyte-derived APC |pdf=|usr=}}{{12517968}} gab.com Text Autocrine type I IFN and contact with endothelium promote the presentation of influenza A virus by monocyte-derived APC JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=12517968 #FOAvip Purified monocytes infected with influenza A virus do not become mature dendritic cells (DCs) and they present viral peptides poorly to autologous memory T cells. In this study, we investigated whether influenza A-infected monocytes matured to DCs with a high capacity to stimulate T cells when they were infected with influenza A virus in a model tissue setting wherein they were cocultured with endothelium grown on a type I collagen matrix. Intercellular interactions with endothelium strongly promoted the Ag-presenting capacity of monocyte-derived cells infected with influenza A virus, and the heterologous coculture system also enhanced production of IFN-alpha by monocytes in the absence of plasmacytoid cells. Production of IFN-alpha in the presence of endothelium correlated with monocyte differentiation to mature DCs and their ability to stimulate proliferation and IFN-gamma production by autologous T cells. Monocyte-derived cells that developed into migratory DCs promoted proliferation of influenza A virus-specific CD4(+) and CD8(+) cells, whereas those that developed into macrophages promoted proliferation of CD8(+) T cells only. This onset of APC activity could be partially blocked with Ab to the IFN-alphabeta receptor when monocytes were infected with UV-treated virus, but neutralizing this pathway was inconsequential when monocytes were infected with live virus. Thus, type I IFN and direct contact with endothelium promote development of influenza A virus-presenting activity in monocyte-derived cells in a setting in which this differentiation does not depend on plasmacytoid cells. However, when infected with live influenza virus, the role of type I IFN in mediating differentiation and Ag-presenting capacity is expendable, apparently due to other mechanisms of virus-mediated activation. Twit Text FOAVip Autocrine type I IFN and contact with endothelium promote the presentation of influenza A virus by monocyte-derived APC ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=12517968 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=12517968 #FOAvip English Wikipedia <ref>{{Cite pmid|12517968}}</ref> Autocrine type I IFN and contact with endothelium promote the presentation of influenza A virus by monocyte-derived APC #MMPMID12517968 Qu C; Moran TM; Randolph GJ J Immunol 2003[Jan]; 170 (2): 1010-8 PMID12517968show ga Purified monocytes infected with influenza A virus do not become mature dendritic cells (DCs) and they present viral peptides poorly to autologous memory T cells. In this study, we investigated whether influenza A-infected monocytes matured to DCs with a high capacity to stimulate T cells when they were infected with influenza A virus in a model tissue setting wherein they were cocultured with endothelium grown on a type I collagen matrix. Intercellular interactions with endothelium strongly promoted the Ag-presenting capacity of monocyte-derived cells infected with influenza A virus, and the heterologous coculture system also enhanced production of IFN-alpha by monocytes in the absence of plasmacytoid cells. Production of IFN-alpha in the presence of endothelium correlated with monocyte differentiation to mature DCs and their ability to stimulate proliferation and IFN-gamma production by autologous T cells. Monocyte-derived cells that developed into migratory DCs promoted proliferation of influenza A virus-specific CD4(+) and CD8(+) cells, whereas those that developed into macrophages promoted proliferation of CD8(+) T cells only. This onset of APC activity could be partially blocked with Ab to the IFN-alphabeta receptor when monocytes were infected with UV-treated virus, but neutralizing this pathway was inconsequential when monocytes were infected with live virus. Thus, type I IFN and direct contact with endothelium promote development of influenza A virus-presenting activity in monocyte-derived cells in a setting in which this differentiation does not depend on plasmacytoid cells. However, when infected with live influenza virus, the role of type I IFN in mediating differentiation and Ag-presenting capacity is expendable, apparently due to other mechanisms of virus-mediated activation. |*Antigen Presentation/immunology/physiology[MESH] |Adult[MESH] |Antigen-Presenting Cells/cytology/*immunology/metabolism/virology[MESH] |Autocrine Communication/*immunology[MESH] |Cell Communication/*immunology/physiology[MESH] |Cell Differentiation/immunology[MESH] |Cells, Cultured[MESH] |Coculture Techniques[MESH] |Endothelium, Vascular/cytology/*immunology/virology[MESH] |Fetal Blood[MESH] |Granulocyte-Macrophage Colony-Stimulating Factor/biosynthesis[MESH] |Humans[MESH] |Influenza A virus/*immunology[MESH] |Interferon Type I/biosynthesis/*physiology[MESH] |Interferon-alpha/biosynthesis/physiology[MESH]Autocrine type I IFN and contact with endothelium promote the presenta(epmc).pdf DeepDyve Pubget Overpricing