Toll-Like Receptor 4-Dependent Activation of Dendritic Cells by a Retrovirus

Burzyn, Dalia; Rassa, John C.; Kim, David; Nepomnaschy, Irene; Ross, Susan R.; Piazzon, Isabel

doi:10.1128/jvi.78.2.576-584.2004

Cited by 117 publications

(95 citation statements)

References 49 publications

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“…This synergy can also be explained by our findings that highlight the ability of TLR3 and TLR4-activated pathways to induce, in a type I IFN-dependent manner, sensors normally absent in iDC and ensuring in this way that powerful effectors will be generated to respond combinatorially to microbial products in different cellular compartments. Another explanation supporting this hypothesis is that TLR4 can participate in the immune response to certain viruses (62)(63)(64)(65)(66)(67); the virus-induced triggering of TLR4 can mediate the transcriptional activation of certain genes encoding intracellular sensors for viruses, such as TLR7, to amplify the response to specific viral infections.…”

Section: Discussionmentioning

confidence: 93%

Sensitization to TLR7 Agonist in IFN-β-Preactivated Dendritic Cells

Severa

Remoli

Giacomini

et al. 2007

The Journal of Immunology

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TLRs interact with a growing list of pathogen-derived products and these interactions drive the activation of innate and adaptive immune responses. Dendritic cells (DC) play a key role in these events expressing a heterogeneous repertoire of TLRs. We have previously demonstrated the production of type I IFNs in DC following bacterial infections and TLR triggering. In this study, we sought to characterize the transcriptome specifically induced in human DC by IFN-β production stimulated upon LPS treatment. To this aim, by using cDNA microarrays, we compared the transcriptome of DC following LPS treatment in the absence or presence of neutralizing anti-type I IFN Abs. Interestingly, we found that the expression of TLR7 was induced during LPS-induced maturation of DC in a type I IFN-dependent manner. The induction of TLR7 in maturing DC was mainly a consequence of the transcriptional activity of IRF-1, whose binding site was located within TLR7 promoter. Moreover, we also demonstrated that “priming” of immature DC, that usually express TLR8 but not TLR7, with exogenous IFN-β induced a functionally active TLR7. In fact, treatment with the TLR7-specific ligand 3M-001 up-regulated the expression of CD83, CD86, and CD38 in IFN-β-primed DC but not in immature DC. Therefore, a robust enhancement in proinflammatory as well as regulatory cytokines was observed. These data suggest that TLR4-mediated type I IFN release activates specific transcription programs in DC amplifying the expression of pathogen sensors to correctly and combinatorially respond to a bacterial as well as viral infection.

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Section: Discussionmentioning

confidence: 93%

Sensitization to TLR7 Agonist in IFN-β-Preactivated Dendritic Cells

Severa

Remoli

Giacomini

et al. 2007

The Journal of Immunology

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“…These authors speculate that TLR4 activation by Env may have a positive effect on viral replication by directly activating B cells, allowing an initial round of viral replication or feedback of TLR4-induced cytokines, which may promote provirus transcription. A recent study has revealed that MMTV activation of TLR4 on dendritic cells enhances expression of its entry receptor, CD71 (14), which suggests that activation of TLR4 by MMTV facilitates viral entry in addition to the replication-enhancing effects described above. This report also showed that TLR2 is activated by MMTV and that TLR2 responses may contribute to these processes (14).…”

Section: Molecular Basis Of Tlr Activationmentioning

confidence: 99%

“…A recent study has revealed that MMTV activation of TLR4 on dendritic cells enhances expression of its entry receptor, CD71 (14), which suggests that activation of TLR4 by MMTV facilitates viral entry in addition to the replication-enhancing effects described above. This report also showed that TLR2 is activated by MMTV and that TLR2 responses may contribute to these processes (14).…”

Section: Molecular Basis Of Tlr Activationmentioning

confidence: 99%

Innate Sensing of Viruses by Toll-Like Receptors

Boehme

Compton

2004

J Virol

233

199

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“…18 Interestingly, the Tf-R (type I, CD71) has been described to be the cell entry receptor for mouse 21 and to play a determining role in the activation of dendritic cells by this retrovirus. 22 This receptor regulates iron uptake not only in reticulocytes but in most cells. 23 As shown in Figure 3d, the TSAP6À/À BMDCs express higher levels of Tf-R than their WT counterparts.…”

Section: Tsap6mentioning

confidence: 99%

Exosome secretion, including the DNA damage-induced p53-dependent secretory pathway, is severely compromised in TSAP6/Steap3-null mice

et al. 2008

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TSAP6 (tumor suppressor-activated pathway 6), also known as Steap3, is a direct p53 transcriptional target gene. It regulates protein secretion, for example translationally controlled tumor protein (TCTP), which is implicated in tumor reversion. In keeping with the latter, we show herein that TSAP6 is a glycosylated protein present in the trans-Golgi network, endosomal-vesicular compartment and cytoplasmic membrane. To further investigate the physiological function of TSAP6, we have generated TSAP6-deficient mice. These mice exhibit microcytic anemia with abnormal reticulocyte maturation and deficient transferrin receptor downregulation, a process known to be dependent on exosomal secretion. Moreover, we provide direct evidence that exosome production is severely compromised in TSAP6-null cells. Finally, we show that the DNA damage-induced p53-dependent nonclassical exosomal secretory pathway is abrogated in TSAP6-null cells. Given the fact that exosomes are used as cell-free vaccines against cancer and that they could be involved in the biogenesis and spread of human immunodeficiency virus, it is important to understand their regulation. The results presented here provide the first genetic demonstration that exosome formation is a tightly controlled biological process dependent of TSAP6.

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Toll-Like Receptor 4-Dependent Activation of Dendritic Cells by a Retrovirus

Abstract: Mouse mammary tumor virus (MMTV) is

Cited by 117 publications

References 49 publications

Sensitization to TLR7 Agonist in IFN-β-Preactivated Dendritic Cells

Sensitization to TLR7 Agonist in IFN-β-Preactivated Dendritic Cells

Innate Sensing of Viruses by Toll-Like Receptors

Exosome secretion, including the DNA damage-induced p53-dependent secretory pathway, is severely compromised in TSAP6/Steap3-null mice

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