Human natural interferon-α producing cells

Fitzgerald-Bocarsly, Patricia

doi:10.1016/0163-7258(93)90021-5

Cited by 198 publications

(154 citation statements)

References 106 publications

(111 reference statements)

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“…In a collaborative study with M. O'Keeffe, K. Shortman and others, we have confirmed responsiveness of purified splenic plasmacytoid pre-DCs to BPL-inactivated influenza virus and shown a lack of response to poly(I)?poly(C) (O'Keeffe et al, 2002), consistent with previous studies indicating that the viral stimulus for the splenic IPC is provided by the viral glycoproteins rather than by dsRNA (Fitzgerald-Bocarsly, 1993;Ito, 1994). The ability to work with defined populations of murine plasmacytoid pre-DCs should facilitate further study of the triggering receptor(s) and possible inhibitory receptor(s) involved in the IFN-a/b response to inactivated influenza virus and the existence of common or distinct pathways of stimulation by other enveloped viruses and microbial stimuli.…”

Section: Discussionsupporting

confidence: 74%

“…A second pathway of IFN-a/b induction that is independent of virus replication or gene expression is seen in the response of certain cells of haemopoietic origin to enveloped viruses. These so-called 'natural' IFN-producing cells (IPCs), found in human and porcine peripheral blood and mouse spleen, produce type 1 IFN in response to physically and chemically inactivated virus, to fixed virusinfected cells, or to cells transfected with particular viral glycoproteins (Fitzgerald-Bocarsly, 1993;Ito, 1994). This IFN-inducing activity has been described for a range of enveloped viruses including herpes-, lenti-, rhabdo-, corona-, orthomyxo-and paramyxoviruses and appears to result from a direct interaction of viral glycoproteins with the surface of the IPC (Charley & Laude, 1988; FitzgeraldBocarsly, 1993;Feldman et al, 1994).…”

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confidence: 99%

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Virus–cell interactions in the induction of type 1 interferon by influenza virus in mouse spleen cells

Miller

Anders

2003

Journal of General Virology

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Inactivated influenza A virus and fixed, virus-infected cells induce type 1 interferon (IFN-a/b) production in murine splenocytes. In this study, we have explored the nature of the virus-spleen cell interaction that leads to IFN-a/b induction and the reason for the poor response to some virus strains. IFN-a/b induction by horse serum-sensitive, but not -resistant, strains of influenza virus was inhibited in the presence of horse serum, indicating that binding of the virus to sialylated cell receptors is a necessary step in the induction process. Furthermore, influenza viruses A/PR/8/34 (H1N1) and A/WS/33 (H1N1), which were poor inducers of IFN-a/b in spleen cells, were shown to have a more active neuraminidase than strains that induced higher IFN levels, and IFN-a/b induction by A/PR/8/34 (H1N1) and A/WS/33 (H1N1) was restored in the presence of a neuraminidase inhibitor. Growth of virus in different cell types altered the level of IFN-a/b induced in spleen cells by particular virus strains, suggesting that the nature of the carbohydrate moieties on the viral glycoproteins may also influence IFN-a/b induction in this system. Consistent with this notion, treatment of egg-grown virus with periodate to oxidize viral carbohydrate greatly reduced its capacity for IFN-a/b induction. Furthermore, induction of IFN-a/b was inhibited in the presence of the saccharides yeast mannan and laminarin. Together these findings indicate: (i) a requirement for interaction of the virus with sialylated receptors on the IFN-producing cell; (ii) an influence of viral carbohydrate on the response; and (iii) possible involvement of a lectin-like receptor on the IFN-producing cell in the induction of IFN-a/b or in regulation of this response. INTRODUCTIONThe type 1 interferons (IFN-a and -b) are key components of antiviral host defence and modulators of the immune system. Produced within hours of viral infection, IFN-a/b induces an antiviral state in uninfected cells (Isaacs & Lindenmann, 1957) that helps to contain spread of the virus (Muller et al., 1994). IFN-a/b also activates natural killer cells and macrophages (Biron et al., 1999;Bogdan, 2000), promotes the maturation and activation of dendritic cells (DCs) (Luft et al., 1998;Gallucci et al., 1999;), and displays potent adjuvant activity for T and B cell responses in vivo (Le Bon et al., 2001).Many cell types can produce IFN-a/b in response to virus infection. Double-stranded RNA (dsRNA) synthesized during the virus replicative cycle (Jacobs & Langland, 1996) is considered a likely trigger, since synthetic dsRNA, e.g. polyinosinic-polycytidylic acid [poly(I)?poly(C)] is known to be a potent inducer of type 1 IFN (De Clercq, 1981). A second pathway of IFN-a/b induction that is independent of virus replication or gene expression is seen in the response of certain cells of haemopoietic origin to enveloped viruses. These so-called 'natural' IFN-producing cells (IPCs), found in human and porcine peripheral blood and mouse spleen, produce type 1 IFN in response to physically and chemical...

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Section: Discussionsupporting

confidence: 74%

mentioning

confidence: 99%

Virus–cell interactions in the induction of type 1 interferon by influenza virus in mouse spleen cells

Miller

Anders

2003

Journal of General Virology

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“…A progressive loss of IFN-␣-producing cells has also been observed in patients with other hematologic disorders, including hairy cell leukemia and idiopathic CD4 lymphopenia, and in patients with HIV infection, though in HIV this decrease could be related to a loss of dendritic cells from viral infection. 35,36 It remains to be determined whether a diminution in dendritic cell numbers in the circulation reflects elimination of these cells or a different pattern of dendritic cell trafficking in SzS patients. Contrary to dendritic cell populations, the number of CD14 ϩ monocytes was not significantly decreased in the blood of patients with advanced CTCL in comparison with those in healthy age-matched donors.…”

Section: Discussionmentioning

confidence: 99%

Sézary syndrome patients demonstrate a defect in dendritic cell populations: effects of CD40 ligand and treatment with GM-CSF on dendritic cell numbers and the production of cytokines

Wysocka

Zaki

French

et al. 2002

Blood

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“…Human PDC also express blood DC antigen 2 (BDCA-2) and BDCA-4, which are an endocytic C-type lectin receptor and neuropilin-1, respectively (10). PDC produce vast amounts of IFN-␣ (3 to 10 pg/cell or 1 to 2 IU/cell) in response to enveloped viruses such as HSV and Sendai virus (SV), in addition to some bacteria and DNA-containing unmethylated CpG sequences (4,7,15,16,25,41). In addition, PDC have been shown to produce inflammatory chemokines such as macrophage inflammatory protein 1␣ (MIP-1␣) and MIP-1␤, IFNinducible protein 10 (IP-10) and MCP-1 in response to CpG, inactivated influenza virus, CD40L stimulation, and HSV stimulation (28,34), and HSV-stimulated PDC express chemokines that attract both natural killer (NK) cells and activated T cells (28).…”

Section: Plasmacytoid Dendritic Cells (Pdc) Are Potent Producers Of Amentioning

confidence: 99%

Characterization of Virus-Responsive Plasmacytoid Dendritic Cells in the Rhesus Macaque

Chung

Amrute

Abel

et al. 2005

Clin Vaccine Immunol

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Plasmacytoid dendritic cells (PDC) are potent producers of alpha interferon (IFN-␣In this study, we demonstrate that peripheral blood PDC from healthy macaques are both phenotypically and functionally similar to human PDC and that reagents used for human studies can be used to study macaque PDC. Both human and macaque PBMC expressed IFN-␣ in response to herpes simplex virus (HSV), the prototypical activator of PDC, as measured by using an IFN bioassay and IFN-␣-specific enzyme-linked immunospot assays. Similar to human PDC, macaque PDC were identified by using flow cytometry as CD123 ؉ HLA-DR ؉ lineage ؊ cells. In addition, like human PDC, macaque PDC expressed intracellular IFN-␣, tumor necrosis factor alpha, macrophage inflammatory protein 1␤/CCL4, and IFN-inducible protein 10/CXCL10 upon stimulation with HSV, all as determined by intracellular flow cytometry. We found that IFN regulatory factor 7, which is required for the expression of IFN-␣ genes, was, similar to human PDC, expressed at high levels in macaque PDC compared to monocytes and CD8 ؉ T cells. These findings establish the phenotypic and functional similarity of human and macaque PDC and confirm the utility of tools developed for studying human PDC in this animal model.

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Human natural interferon-α producing cells

Cited by 198 publications

References 106 publications

Virus–cell interactions in the induction of type 1 interferon by influenza virus in mouse spleen cells

Virus–cell interactions in the induction of type 1 interferon by influenza virus in mouse spleen cells

Sézary syndrome patients demonstrate a defect in dendritic cell populations: effects of CD40 ligand and treatment with GM-CSF on dendritic cell numbers and the production of cytokines

Characterization of Virus-Responsive Plasmacytoid Dendritic Cells in the Rhesus Macaque

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