Antibody-Dependent Induction of Type I Interferons by Poliovirus in Human Mononuclear Blood Cells Requires the Type II Fcγ Receptor (CD32)

Palmer, Pierre; Charley, Bernard; Rombaut, Bartholomeus; Daëron, Marc; Lebon, Pierre

doi:10.1006/viro.2000.0627

Cited by 57 publications

(53 citation statements)

References 35 publications

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“…Stimulatory concentrations of PG, for example, were only reached with proliferating bacteria. A similar observation was made by several groups working on viral pDC activation via nucleic acids that seemed to be dependent on viral replication (26,57,70). Therefore, ongoing bacterial DNA and RNA synthesis may represent a prerequisite for passing the threshold concentration of nucleic acids necessary for TLR stimulation.…”

Section: Discussionsupporting

confidence: 69%

Staphylococcus aureus-Induced Plasmacytoid Dendritic Cell Activation Is Based on an IgG-Mediated Memory Response

Parčina

Wendt

Goetz

et al. 2008

The Journal of Immunology

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Type I IFNs represent a major antimicrobial defense mechanism due to their property of enhancing immune responses by priming both innate and adaptive immune cells. Plasmacytoid dendritic cells (pDC) are the major source of type I IFN in the human body and represent innate immune cells involved in first-line defense against invading pathogens. Although pDC activation has been extensively studied upon stimulation with synthetic TLR ligands, viruses, and intracellular bacteria, there is only scarce information on extracellular bacteria. In this study we show that the triggering of human pDC-derived IFN-α secretion by Staphylococcus aureus is independent of TLR2 and specific for coagulase-positive staphylococci. Specificity of the pDC response to S. aureus is independent of the bacterial virulence factors protein A and α-toxin but is mediated by Ag-specific IgG and CD32. S. aureus-induced pDC activation can be blocked by inhibitory DNA oligonucleotides and chloroquine, suggesting that engagement of TLR7/9 by bacterial nucleic acids after CD32-mediated uptake of these compounds may play a central role in this process. Altogether, we propose that in marked contrast to nonselective TLR2-dependent activation of most innate immune cells, pDC activation by S. aureus represents an Ag-specific memory response since it requires the presence of class-switched immunoglobulins.

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Section: Discussionsupporting

confidence: 69%

Staphylococcus aureus-Induced Plasmacytoid Dendritic Cell Activation Is Based on an IgG-Mediated Memory Response

Parčina

Wendt

Goetz

et al. 2008

The Journal of Immunology

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“…This contrasts with other viruses, such as HIV and poliovirus, with which antibody complexing had a positive effect on the induction of IFN-a production by PBMC [25,26].…”

Section: Discussioncontrasting

confidence: 58%

FcγRII-dependent sensitisation of natural interferon-producing cells for viral infection and interferon-α responses

Balmelli¹,

Vincent²,

Rau³

et al. 2005

Eur. J. Immunol.

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Natural interferon-producing cells (NIPC), also called plasmacytoid dendritic cells, are the most potent producers of IFN-a in response to viral and bacterial components,s serving an important function in innate immune defences. The present work demonstrates that NIPC responsiveness can be primed by immunisation, increasing their capacity to produce IFN-a after viral infection. NIPC isolated from pigs immunised against classical swine fever virus (CSFV), a member of the Flaviviridae, were more receptive to viral infection and produced higher levels of IFN-a than NIPC from immunologically naive animals. This sensitisation of NIPC was maintained for at least 8 months after immunisation. IFN-a production was dependent on live virus and required replication, and the "immune" NIPC responded to lower infectious doses of virus. Co-localisation of the virus with FccRII (CD32) in polarised structures was observed with "immune" NIPC only. This FccRII-dependent virus capture and sensitisation of NIPC, evidently mediated through cytophilic CSFV-specific antibodies, was inhibited by non-specifically aggregated immunoglobulin as well as by pre-formed virus-antibody complexes. In conclusion, these results demonstrate that NIPC not only represent a major player in innate immunity but are also functionally linked to the immunological memory of the adaptive immune system.

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“…This cellular duo can be further stimulated with immune complexes (Ab-RNA/DNA, Abviruses), and therefore represents a crucial player in the initiation and amplification of antimicrobial responses as well as the propagation of autoimmune diseases such as systemic lupus erythematosus. [9][10][11] More detailed studies on human B-cell populations have shown that peripheral blood-derived naive and memory B cells express distinct levels of TLR6, 7, and 9. Indeed, TLR6, 7, 9, and 10 are barely expressed by circulating naive B cells, 7 whereas memory B cells display a higher sensitivity to TLR activation with a concomitant higher capacity for differentiation into plasma cells.…”

Section: Tlr Expression In Normal and Neoplastic B Cells Normal B-celmentioning

confidence: 99%

Toll-like receptors: lessons to learn from normal and malignant human B cells

Chiron

Bekeredjian‐Ding

Pellat‐Deceunynck

et al. 2008

Blood

103

104

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IntroductionThe human immune system is continuously challenged by commensal microflora as well as invasive infectious agents. The decision to mount a rapid and protective immune response to a pathogen is a consequence of the activation of the innate immune system via pattern recognition receptors, such as Toll-like receptors (TLRs), that sense microbial products. 1 TLR polymorphisms have been implicated in increased severity and predisposition to infection and septic shock 2 in both mice and humans. TLRs recognize highly conserved structures of viral (TLR3,7,8,and 9) and bacterial (TLR1,2,4,5,6,7,8,and 9) origin, known as pathogen-associated molecular patterns (PAMPs; Figure 1). TLR2 heterodimerization with TLR1 or TLR6 is triggered by bacterial lipopeptides, whereas TLR3 is activated by double-stranded RNA, TLR4 is activated by lipopolysaccharide (LPS), TLR5 is activated by flagellin, TLR7 and TLR8 are activated by single-stranded RNA (ssRNA), and TLR9 is activated by unmethylated CpG DNA motifs. Moreover, endogenous ligands released during cellular stress or matrix degradation (eg, heat-shock proteins, fibronectin, heparan sulfates) are thought to activate TLRs. 3 Numerous reports have described how TLRs orchestrate the immune response to pathogens in dendritic cells (DCs) and macrophages. 4 Much less is known about the effects of TLR-mediated B-cell activation, although the design of vaccines could benefit from a more detailed understanding of this process.Leukemic B cells often retain the expression of markers specific for their cellular origin (eg, CD5, CD10, CD138). Furthermore, several reports have demonstrated TLR expression and function in neoplastic B cells. Because DCs can be activated and matured upon triggering of TLRs, immunotherapeutic protocols in leukemia have recently included TLR agonists to improve tumor antigen presentation and subsequent T-cell activation. 5 However, recent reports have indicated that leukemic cells could hijack the TLR machinery to their own benefit. A better understanding of the effects of TLR ligands on normal B cells and their leukemic counterparts could therefore help avoid adverse vaccination effects. In this review, we will discuss the role of TLRs in generating the humoral immune response and their dual effects on different leukemic cell types. TLR expression in normal and neoplastic B cells Normal B-cell subsets and modulation of expressionThe TLR expression pattern is specific for each cell type and is summarized in Figure 2 for human B cells. TLRs expression in human B cells is characterized by high expression of TLR1, 6, 7, 9, and 10. 6-8 Low expression of TLR2 allows for the formation of the functional heterodimers TLR1/2 and TLR2/6, which are required to respond to diacylated and triacylated lipoproteins. The inability to be activated by LPS is a hallmark of human B cells because they lack TLR4, in contrast to mouse B cells. However, human B cells are well equipped to recognize nucleic acids given their expression of TLR7 and TLR9. This profile allows them to ...

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Antibody-Dependent Induction of Type I Interferons by Poliovirus in Human Mononuclear Blood Cells Requires the Type II Fcγ Receptor (CD32)

Cited by 57 publications

References 35 publications

Staphylococcus aureus-Induced Plasmacytoid Dendritic Cell Activation Is Based on an IgG-Mediated Memory Response

Staphylococcus aureus-Induced Plasmacytoid Dendritic Cell Activation Is Based on an IgG-Mediated Memory Response

FcγRII-dependent sensitisation of natural interferon-producing cells for viral infection and interferon-α responses

Toll-like receptors: lessons to learn from normal and malignant human B cells

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