The role of type I interferons in non‐viral infections

Bogdan, Christian; Mattner, Jochen; Schleicher, Ulrike

doi:10.1111/j.0105-2896.2004.00207.x

Cited by 151 publications

(142 citation statements)

References 233 publications

(265 reference statements)

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“…IFNIs are among the earliest cytokines that are induced during infection and play an important regulatory role in both innate and adaptive immune responses (3). IFNIs are able to activate macrophages (4), enhance cytolytic activity of NK cells (5), and promote IFN-␥ secretion and Th1 differentiation (5). In particular, IFNIs can activate and modulate the function of dendritic cells (DCs), the most important APCs, via promoting MHC expression, costimulatory molecule expression, and cytokine/chemokine secretion, thus modulating adaptive T cell immune responses (3, 6 -9).…”

Section: T He Group Of Type I Ifns (Ifnis)mentioning

confidence: 99%

Type I IFNs Enhance Susceptibility toChlamydia muridarumLung Infection by Enhancing Apoptosis of Local Macrophages

Qiu

Fan

Joyee

et al. 2008

The Journal of Immunology

112

110

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Type I IFNs (IFNIs) have pleiotropic functions in regulating host innate and adaptive immune responses to pathogens. To elucidate the role of IFNIs in host resistance to chlamydial infection in vivo, we compared IFN-α/β receptor knockout (IFNAR−/−) and wild-type control mice in susceptibility to Chlamydia trachomatis mouse pneumonitis (Chlamydia muridarum) lung infection. We found that the IFNAR−/− mice were significantly more resistant to C. muridarum infection showing less bacterial burden and bodyweight loss, and milder pathological changes. However, IFN-γ response, which is believed to be critical in host defense against chlamydial infection, was similar between the wild-type and IFNAR−/− mice. More importantly, TUNEL analysis showed less macrophage apoptosis in IFNAR−/− mice, which was consistent with lower expressions of IFNI-induced apoptotic factors, TRAIL, Daxx, and PKR. Furthermore, depletion of lung macrophages with dichloromethylene diphosphonate-liposome significantly increased the susceptibility of the IFNAR−/− mice to C. muridarum, confirming the importance of macrophages. Overall, the data indicate that IFNIs play a promoting role in C. muridarum lung infection, largely through increase of local macrophage apoptosis.

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Section: T He Group Of Type I Ifns (Ifnis)mentioning

confidence: 99%

Type I IFNs Enhance Susceptibility toChlamydia muridarumLung Infection by Enhancing Apoptosis of Local Macrophages

Qiu

Fan

Joyee

et al. 2008

The Journal of Immunology

112

110

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“…In marked contrast to viral infection, little is known about the role of pDC in bacterial infection (29,30). There are a few studies available that state that intracellular bacteria such as chlamydia, salmonella, mycobacteria, and listeria can induce type I IFN production (31)(32)(33)(34)(35)(36), while even fewer reports observe type I IFN secretion in response to extracellular bacteria including Staphylococcus aureus and Escherichia coli (37)(38)(39)(40).…”

Section: P Lasmacytoid Dendritic Cells (Pdc)mentioning

confidence: 99%

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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“…Type I interferons (IFNs) are pleiotropic cytokines that possess several biological activities and play a central role in basic and applied research as mediators of antiviral and antigrowth responses, modulators of the immune system, and therapeutic agents against viral diseases and cancer [4,5].…”

Section: Introductionmentioning

confidence: 99%

KAP1 regulates type I interferon/STAT1-mediated IRF-1 gene expression

Kamitani

Ohbayashi

Ikeda

et al. 2008

Biochemical and Biophysical Research Communications

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Signal transducers and activators of transcription (STATs) mediate cell proliferation, differentiation, and survival in immune responses, hematopoiesis, neurogenesis, and other biological processes.Recently, we showed that KAP1 is a novel STAT-binding partner that regulates STAT3-mediated transactivation. KAP1 is a universal corepressor protein for the KRAB zinc finger protein superfamily of transcriptional repressors. In this study, we found KAP1-dependent repression of interferon (IFN) /STAT1-mediated signaling. We also demonstrated that endogenous KAP1 associates with endogenous STAT1 in vivo. Importantly, a small-interfering RNA-mediated reduction in KAP1 expression enhanced IFN-induced STAT1-dependent IRF-1 gene expression.These results indicate that KAP1 may act as an endogenous regulator of the IFN/STAT1 signaling pathway.

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The role of type I interferons in non‐viral infections

Cited by 151 publications

References 233 publications

Type I IFNs Enhance Susceptibility toChlamydia muridarumLung Infection by Enhancing Apoptosis of Local Macrophages

Type I IFNs Enhance Susceptibility toChlamydia muridarumLung Infection by Enhancing Apoptosis of Local Macrophages

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

KAP1 regulates type I interferon/STAT1-mediated IRF-1 gene expression

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