188
The rapid host response to virus infection is crucial for establishment of the antiviral state and for the release of pro-inflammatory mediators that coordinate the adaptive immune response. Induction of antiviral and inflammatory genes is achieved largely through recognition of viral nucleic acid m...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Olagnier, David [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2013transfer abstract |
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| Übergeordnetes Werk: |
Enthalten in: The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types - McLaughlin, Richard J. ELSEVIER, 2022, the official journal of the International Cytokine Society, Oxford [u.a.] |
|---|---|
| Übergeordnetes Werk: |
volume:63 ; year:2013 ; number:3 ; pages:287 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.cyto.2013.06.191 |
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ELV022162984 |
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| 520 | |a The rapid host response to virus infection is crucial for establishment of the antiviral state and for the release of pro-inflammatory mediators that coordinate the adaptive immune response. Induction of antiviral and inflammatory genes is achieved largely through recognition of viral nucleic acid motifs by pattern recognition receptors. Dengue virus (DENV) is a significant human pathogen that causes a wide spectrum of clinical symptoms, ranging from mild dengue fever to severe hemorrhagic fever and shock syndrome. The cytosolic receptors RIG-I/MDA5 as well as the membrane-bound TLR3/TLR7 localized in the endosomes are important sensors of DENV infection. The role of reactive oxygen species (ROS) in the activation of biological processes such as autophagy, necrosis, and inflammasome activation adds another layer of complexity to the regulation of immune sensing. Transcriptome analysis of DENV-infected human monocyte-derived dendritic cells (Mo-DC) revealed the activation of distinct patterns of gene transcription, with involvement of pathways including the antiviral response, the TNF superfamily and late activation of death receptor signaling. Interestingly, a dominant early gene network associated with the Nrf2-dependent antioxidant response was also identified; DENV infection induced an early production of ROS that was dependent on NADPH-oxidase, and was essential for the activation of inflammatory and antiviral programs, through NF-κB and IRF-3 transcription factors, respectively. Using a high throughput qPCR assay, we demonstrated that interfering with NADPH-oxidase inhibited DENV-induced antiviral and inflammatory responses. We also demonstrated that the antioxidant pathway controlled by the transcription factor Nrf2 is a pivotal upstream link to the regulation of DENV-induced antiviral and inflammatory responses under oxidative conditions. In conclusion, these findings demonstrate that ROS production is crucial for effective activation of pathways leading to innate immune responses against DENV infection in human Mo-DC. | ||
| 520 | |a The rapid host response to virus infection is crucial for establishment of the antiviral state and for the release of pro-inflammatory mediators that coordinate the adaptive immune response. Induction of antiviral and inflammatory genes is achieved largely through recognition of viral nucleic acid motifs by pattern recognition receptors. Dengue virus (DENV) is a significant human pathogen that causes a wide spectrum of clinical symptoms, ranging from mild dengue fever to severe hemorrhagic fever and shock syndrome. The cytosolic receptors RIG-I/MDA5 as well as the membrane-bound TLR3/TLR7 localized in the endosomes are important sensors of DENV infection. The role of reactive oxygen species (ROS) in the activation of biological processes such as autophagy, necrosis, and inflammasome activation adds another layer of complexity to the regulation of immune sensing. Transcriptome analysis of DENV-infected human monocyte-derived dendritic cells (Mo-DC) revealed the activation of distinct patterns of gene transcription, with involvement of pathways including the antiviral response, the TNF superfamily and late activation of death receptor signaling. Interestingly, a dominant early gene network associated with the Nrf2-dependent antioxidant response was also identified; DENV infection induced an early production of ROS that was dependent on NADPH-oxidase, and was essential for the activation of inflammatory and antiviral programs, through NF-κB and IRF-3 transcription factors, respectively. Using a high throughput qPCR assay, we demonstrated that interfering with NADPH-oxidase inhibited DENV-induced antiviral and inflammatory responses. We also demonstrated that the antioxidant pathway controlled by the transcription factor Nrf2 is a pivotal upstream link to the regulation of DENV-induced antiviral and inflammatory responses under oxidative conditions. In conclusion, these findings demonstrate that ROS production is crucial for effective activation of pathways leading to innate immune responses against DENV infection in human Mo-DC. | ||
| 700 | 1 | |a Nichols, Carmen |4 oth | |
| 700 | 1 | |a He, Zhong |4 oth | |
| 700 | 1 | |a Hiscott, John |4 oth | |
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10.1016/j.cyto.2013.06.191 doi GBVA2013017000028.pica (DE-627)ELV022162984 (ELSEVIER)S1043-4666(13)00465-1 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 44.83 bkl Olagnier, David verfasserin aut 188 2013transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The rapid host response to virus infection is crucial for establishment of the antiviral state and for the release of pro-inflammatory mediators that coordinate the adaptive immune response. Induction of antiviral and inflammatory genes is achieved largely through recognition of viral nucleic acid motifs by pattern recognition receptors. Dengue virus (DENV) is a significant human pathogen that causes a wide spectrum of clinical symptoms, ranging from mild dengue fever to severe hemorrhagic fever and shock syndrome. The cytosolic receptors RIG-I/MDA5 as well as the membrane-bound TLR3/TLR7 localized in the endosomes are important sensors of DENV infection. The role of reactive oxygen species (ROS) in the activation of biological processes such as autophagy, necrosis, and inflammasome activation adds another layer of complexity to the regulation of immune sensing. Transcriptome analysis of DENV-infected human monocyte-derived dendritic cells (Mo-DC) revealed the activation of distinct patterns of gene transcription, with involvement of pathways including the antiviral response, the TNF superfamily and late activation of death receptor signaling. Interestingly, a dominant early gene network associated with the Nrf2-dependent antioxidant response was also identified; DENV infection induced an early production of ROS that was dependent on NADPH-oxidase, and was essential for the activation of inflammatory and antiviral programs, through NF-κB and IRF-3 transcription factors, respectively. Using a high throughput qPCR assay, we demonstrated that interfering with NADPH-oxidase inhibited DENV-induced antiviral and inflammatory responses. We also demonstrated that the antioxidant pathway controlled by the transcription factor Nrf2 is a pivotal upstream link to the regulation of DENV-induced antiviral and inflammatory responses under oxidative conditions. In conclusion, these findings demonstrate that ROS production is crucial for effective activation of pathways leading to innate immune responses against DENV infection in human Mo-DC. The rapid host response to virus infection is crucial for establishment of the antiviral state and for the release of pro-inflammatory mediators that coordinate the adaptive immune response. Induction of antiviral and inflammatory genes is achieved largely through recognition of viral nucleic acid motifs by pattern recognition receptors. Dengue virus (DENV) is a significant human pathogen that causes a wide spectrum of clinical symptoms, ranging from mild dengue fever to severe hemorrhagic fever and shock syndrome. The cytosolic receptors RIG-I/MDA5 as well as the membrane-bound TLR3/TLR7 localized in the endosomes are important sensors of DENV infection. The role of reactive oxygen species (ROS) in the activation of biological processes such as autophagy, necrosis, and inflammasome activation adds another layer of complexity to the regulation of immune sensing. Transcriptome analysis of DENV-infected human monocyte-derived dendritic cells (Mo-DC) revealed the activation of distinct patterns of gene transcription, with involvement of pathways including the antiviral response, the TNF superfamily and late activation of death receptor signaling. Interestingly, a dominant early gene network associated with the Nrf2-dependent antioxidant response was also identified; DENV infection induced an early production of ROS that was dependent on NADPH-oxidase, and was essential for the activation of inflammatory and antiviral programs, through NF-κB and IRF-3 transcription factors, respectively. Using a high throughput qPCR assay, we demonstrated that interfering with NADPH-oxidase inhibited DENV-induced antiviral and inflammatory responses. We also demonstrated that the antioxidant pathway controlled by the transcription factor Nrf2 is a pivotal upstream link to the regulation of DENV-induced antiviral and inflammatory responses under oxidative conditions. In conclusion, these findings demonstrate that ROS production is crucial for effective activation of pathways leading to innate immune responses against DENV infection in human Mo-DC. Nichols, Carmen oth He, Zhong oth Hiscott, John oth Enthalten in Elsevier McLaughlin, Richard J. ELSEVIER The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types 2022 the official journal of the International Cytokine Society Oxford [u.a.] (DE-627)ELV008219540 volume:63 year:2013 number:3 pages:287 https://doi.org/10.1016/j.cyto.2013.06.191 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.83 Rheumatologie Orthopädie VZ AR 63 2013 3 287 045F 570 |
| spelling |
10.1016/j.cyto.2013.06.191 doi GBVA2013017000028.pica (DE-627)ELV022162984 (ELSEVIER)S1043-4666(13)00465-1 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 44.83 bkl Olagnier, David verfasserin aut 188 2013transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The rapid host response to virus infection is crucial for establishment of the antiviral state and for the release of pro-inflammatory mediators that coordinate the adaptive immune response. Induction of antiviral and inflammatory genes is achieved largely through recognition of viral nucleic acid motifs by pattern recognition receptors. Dengue virus (DENV) is a significant human pathogen that causes a wide spectrum of clinical symptoms, ranging from mild dengue fever to severe hemorrhagic fever and shock syndrome. The cytosolic receptors RIG-I/MDA5 as well as the membrane-bound TLR3/TLR7 localized in the endosomes are important sensors of DENV infection. The role of reactive oxygen species (ROS) in the activation of biological processes such as autophagy, necrosis, and inflammasome activation adds another layer of complexity to the regulation of immune sensing. Transcriptome analysis of DENV-infected human monocyte-derived dendritic cells (Mo-DC) revealed the activation of distinct patterns of gene transcription, with involvement of pathways including the antiviral response, the TNF superfamily and late activation of death receptor signaling. Interestingly, a dominant early gene network associated with the Nrf2-dependent antioxidant response was also identified; DENV infection induced an early production of ROS that was dependent on NADPH-oxidase, and was essential for the activation of inflammatory and antiviral programs, through NF-κB and IRF-3 transcription factors, respectively. Using a high throughput qPCR assay, we demonstrated that interfering with NADPH-oxidase inhibited DENV-induced antiviral and inflammatory responses. We also demonstrated that the antioxidant pathway controlled by the transcription factor Nrf2 is a pivotal upstream link to the regulation of DENV-induced antiviral and inflammatory responses under oxidative conditions. In conclusion, these findings demonstrate that ROS production is crucial for effective activation of pathways leading to innate immune responses against DENV infection in human Mo-DC. The rapid host response to virus infection is crucial for establishment of the antiviral state and for the release of pro-inflammatory mediators that coordinate the adaptive immune response. Induction of antiviral and inflammatory genes is achieved largely through recognition of viral nucleic acid motifs by pattern recognition receptors. Dengue virus (DENV) is a significant human pathogen that causes a wide spectrum of clinical symptoms, ranging from mild dengue fever to severe hemorrhagic fever and shock syndrome. The cytosolic receptors RIG-I/MDA5 as well as the membrane-bound TLR3/TLR7 localized in the endosomes are important sensors of DENV infection. The role of reactive oxygen species (ROS) in the activation of biological processes such as autophagy, necrosis, and inflammasome activation adds another layer of complexity to the regulation of immune sensing. Transcriptome analysis of DENV-infected human monocyte-derived dendritic cells (Mo-DC) revealed the activation of distinct patterns of gene transcription, with involvement of pathways including the antiviral response, the TNF superfamily and late activation of death receptor signaling. Interestingly, a dominant early gene network associated with the Nrf2-dependent antioxidant response was also identified; DENV infection induced an early production of ROS that was dependent on NADPH-oxidase, and was essential for the activation of inflammatory and antiviral programs, through NF-κB and IRF-3 transcription factors, respectively. Using a high throughput qPCR assay, we demonstrated that interfering with NADPH-oxidase inhibited DENV-induced antiviral and inflammatory responses. We also demonstrated that the antioxidant pathway controlled by the transcription factor Nrf2 is a pivotal upstream link to the regulation of DENV-induced antiviral and inflammatory responses under oxidative conditions. In conclusion, these findings demonstrate that ROS production is crucial for effective activation of pathways leading to innate immune responses against DENV infection in human Mo-DC. Nichols, Carmen oth He, Zhong oth Hiscott, John oth Enthalten in Elsevier McLaughlin, Richard J. ELSEVIER The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types 2022 the official journal of the International Cytokine Society Oxford [u.a.] (DE-627)ELV008219540 volume:63 year:2013 number:3 pages:287 https://doi.org/10.1016/j.cyto.2013.06.191 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.83 Rheumatologie Orthopädie VZ AR 63 2013 3 287 045F 570 |
| allfields_unstemmed |
10.1016/j.cyto.2013.06.191 doi GBVA2013017000028.pica (DE-627)ELV022162984 (ELSEVIER)S1043-4666(13)00465-1 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 44.83 bkl Olagnier, David verfasserin aut 188 2013transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The rapid host response to virus infection is crucial for establishment of the antiviral state and for the release of pro-inflammatory mediators that coordinate the adaptive immune response. Induction of antiviral and inflammatory genes is achieved largely through recognition of viral nucleic acid motifs by pattern recognition receptors. Dengue virus (DENV) is a significant human pathogen that causes a wide spectrum of clinical symptoms, ranging from mild dengue fever to severe hemorrhagic fever and shock syndrome. The cytosolic receptors RIG-I/MDA5 as well as the membrane-bound TLR3/TLR7 localized in the endosomes are important sensors of DENV infection. The role of reactive oxygen species (ROS) in the activation of biological processes such as autophagy, necrosis, and inflammasome activation adds another layer of complexity to the regulation of immune sensing. Transcriptome analysis of DENV-infected human monocyte-derived dendritic cells (Mo-DC) revealed the activation of distinct patterns of gene transcription, with involvement of pathways including the antiviral response, the TNF superfamily and late activation of death receptor signaling. Interestingly, a dominant early gene network associated with the Nrf2-dependent antioxidant response was also identified; DENV infection induced an early production of ROS that was dependent on NADPH-oxidase, and was essential for the activation of inflammatory and antiviral programs, through NF-κB and IRF-3 transcription factors, respectively. Using a high throughput qPCR assay, we demonstrated that interfering with NADPH-oxidase inhibited DENV-induced antiviral and inflammatory responses. We also demonstrated that the antioxidant pathway controlled by the transcription factor Nrf2 is a pivotal upstream link to the regulation of DENV-induced antiviral and inflammatory responses under oxidative conditions. In conclusion, these findings demonstrate that ROS production is crucial for effective activation of pathways leading to innate immune responses against DENV infection in human Mo-DC. The rapid host response to virus infection is crucial for establishment of the antiviral state and for the release of pro-inflammatory mediators that coordinate the adaptive immune response. Induction of antiviral and inflammatory genes is achieved largely through recognition of viral nucleic acid motifs by pattern recognition receptors. Dengue virus (DENV) is a significant human pathogen that causes a wide spectrum of clinical symptoms, ranging from mild dengue fever to severe hemorrhagic fever and shock syndrome. The cytosolic receptors RIG-I/MDA5 as well as the membrane-bound TLR3/TLR7 localized in the endosomes are important sensors of DENV infection. The role of reactive oxygen species (ROS) in the activation of biological processes such as autophagy, necrosis, and inflammasome activation adds another layer of complexity to the regulation of immune sensing. Transcriptome analysis of DENV-infected human monocyte-derived dendritic cells (Mo-DC) revealed the activation of distinct patterns of gene transcription, with involvement of pathways including the antiviral response, the TNF superfamily and late activation of death receptor signaling. Interestingly, a dominant early gene network associated with the Nrf2-dependent antioxidant response was also identified; DENV infection induced an early production of ROS that was dependent on NADPH-oxidase, and was essential for the activation of inflammatory and antiviral programs, through NF-κB and IRF-3 transcription factors, respectively. Using a high throughput qPCR assay, we demonstrated that interfering with NADPH-oxidase inhibited DENV-induced antiviral and inflammatory responses. We also demonstrated that the antioxidant pathway controlled by the transcription factor Nrf2 is a pivotal upstream link to the regulation of DENV-induced antiviral and inflammatory responses under oxidative conditions. In conclusion, these findings demonstrate that ROS production is crucial for effective activation of pathways leading to innate immune responses against DENV infection in human Mo-DC. Nichols, Carmen oth He, Zhong oth Hiscott, John oth Enthalten in Elsevier McLaughlin, Richard J. ELSEVIER The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types 2022 the official journal of the International Cytokine Society Oxford [u.a.] (DE-627)ELV008219540 volume:63 year:2013 number:3 pages:287 https://doi.org/10.1016/j.cyto.2013.06.191 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.83 Rheumatologie Orthopädie VZ AR 63 2013 3 287 045F 570 |
| allfieldsGer |
10.1016/j.cyto.2013.06.191 doi GBVA2013017000028.pica (DE-627)ELV022162984 (ELSEVIER)S1043-4666(13)00465-1 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 44.83 bkl Olagnier, David verfasserin aut 188 2013transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The rapid host response to virus infection is crucial for establishment of the antiviral state and for the release of pro-inflammatory mediators that coordinate the adaptive immune response. Induction of antiviral and inflammatory genes is achieved largely through recognition of viral nucleic acid motifs by pattern recognition receptors. Dengue virus (DENV) is a significant human pathogen that causes a wide spectrum of clinical symptoms, ranging from mild dengue fever to severe hemorrhagic fever and shock syndrome. The cytosolic receptors RIG-I/MDA5 as well as the membrane-bound TLR3/TLR7 localized in the endosomes are important sensors of DENV infection. The role of reactive oxygen species (ROS) in the activation of biological processes such as autophagy, necrosis, and inflammasome activation adds another layer of complexity to the regulation of immune sensing. Transcriptome analysis of DENV-infected human monocyte-derived dendritic cells (Mo-DC) revealed the activation of distinct patterns of gene transcription, with involvement of pathways including the antiviral response, the TNF superfamily and late activation of death receptor signaling. Interestingly, a dominant early gene network associated with the Nrf2-dependent antioxidant response was also identified; DENV infection induced an early production of ROS that was dependent on NADPH-oxidase, and was essential for the activation of inflammatory and antiviral programs, through NF-κB and IRF-3 transcription factors, respectively. Using a high throughput qPCR assay, we demonstrated that interfering with NADPH-oxidase inhibited DENV-induced antiviral and inflammatory responses. We also demonstrated that the antioxidant pathway controlled by the transcription factor Nrf2 is a pivotal upstream link to the regulation of DENV-induced antiviral and inflammatory responses under oxidative conditions. In conclusion, these findings demonstrate that ROS production is crucial for effective activation of pathways leading to innate immune responses against DENV infection in human Mo-DC. The rapid host response to virus infection is crucial for establishment of the antiviral state and for the release of pro-inflammatory mediators that coordinate the adaptive immune response. Induction of antiviral and inflammatory genes is achieved largely through recognition of viral nucleic acid motifs by pattern recognition receptors. Dengue virus (DENV) is a significant human pathogen that causes a wide spectrum of clinical symptoms, ranging from mild dengue fever to severe hemorrhagic fever and shock syndrome. The cytosolic receptors RIG-I/MDA5 as well as the membrane-bound TLR3/TLR7 localized in the endosomes are important sensors of DENV infection. The role of reactive oxygen species (ROS) in the activation of biological processes such as autophagy, necrosis, and inflammasome activation adds another layer of complexity to the regulation of immune sensing. Transcriptome analysis of DENV-infected human monocyte-derived dendritic cells (Mo-DC) revealed the activation of distinct patterns of gene transcription, with involvement of pathways including the antiviral response, the TNF superfamily and late activation of death receptor signaling. Interestingly, a dominant early gene network associated with the Nrf2-dependent antioxidant response was also identified; DENV infection induced an early production of ROS that was dependent on NADPH-oxidase, and was essential for the activation of inflammatory and antiviral programs, through NF-κB and IRF-3 transcription factors, respectively. Using a high throughput qPCR assay, we demonstrated that interfering with NADPH-oxidase inhibited DENV-induced antiviral and inflammatory responses. We also demonstrated that the antioxidant pathway controlled by the transcription factor Nrf2 is a pivotal upstream link to the regulation of DENV-induced antiviral and inflammatory responses under oxidative conditions. In conclusion, these findings demonstrate that ROS production is crucial for effective activation of pathways leading to innate immune responses against DENV infection in human Mo-DC. Nichols, Carmen oth He, Zhong oth Hiscott, John oth Enthalten in Elsevier McLaughlin, Richard J. ELSEVIER The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types 2022 the official journal of the International Cytokine Society Oxford [u.a.] (DE-627)ELV008219540 volume:63 year:2013 number:3 pages:287 https://doi.org/10.1016/j.cyto.2013.06.191 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.83 Rheumatologie Orthopädie VZ AR 63 2013 3 287 045F 570 |
| allfieldsSound |
10.1016/j.cyto.2013.06.191 doi GBVA2013017000028.pica (DE-627)ELV022162984 (ELSEVIER)S1043-4666(13)00465-1 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 44.83 bkl Olagnier, David verfasserin aut 188 2013transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The rapid host response to virus infection is crucial for establishment of the antiviral state and for the release of pro-inflammatory mediators that coordinate the adaptive immune response. Induction of antiviral and inflammatory genes is achieved largely through recognition of viral nucleic acid motifs by pattern recognition receptors. Dengue virus (DENV) is a significant human pathogen that causes a wide spectrum of clinical symptoms, ranging from mild dengue fever to severe hemorrhagic fever and shock syndrome. The cytosolic receptors RIG-I/MDA5 as well as the membrane-bound TLR3/TLR7 localized in the endosomes are important sensors of DENV infection. The role of reactive oxygen species (ROS) in the activation of biological processes such as autophagy, necrosis, and inflammasome activation adds another layer of complexity to the regulation of immune sensing. Transcriptome analysis of DENV-infected human monocyte-derived dendritic cells (Mo-DC) revealed the activation of distinct patterns of gene transcription, with involvement of pathways including the antiviral response, the TNF superfamily and late activation of death receptor signaling. Interestingly, a dominant early gene network associated with the Nrf2-dependent antioxidant response was also identified; DENV infection induced an early production of ROS that was dependent on NADPH-oxidase, and was essential for the activation of inflammatory and antiviral programs, through NF-κB and IRF-3 transcription factors, respectively. Using a high throughput qPCR assay, we demonstrated that interfering with NADPH-oxidase inhibited DENV-induced antiviral and inflammatory responses. We also demonstrated that the antioxidant pathway controlled by the transcription factor Nrf2 is a pivotal upstream link to the regulation of DENV-induced antiviral and inflammatory responses under oxidative conditions. In conclusion, these findings demonstrate that ROS production is crucial for effective activation of pathways leading to innate immune responses against DENV infection in human Mo-DC. The rapid host response to virus infection is crucial for establishment of the antiviral state and for the release of pro-inflammatory mediators that coordinate the adaptive immune response. Induction of antiviral and inflammatory genes is achieved largely through recognition of viral nucleic acid motifs by pattern recognition receptors. Dengue virus (DENV) is a significant human pathogen that causes a wide spectrum of clinical symptoms, ranging from mild dengue fever to severe hemorrhagic fever and shock syndrome. The cytosolic receptors RIG-I/MDA5 as well as the membrane-bound TLR3/TLR7 localized in the endosomes are important sensors of DENV infection. The role of reactive oxygen species (ROS) in the activation of biological processes such as autophagy, necrosis, and inflammasome activation adds another layer of complexity to the regulation of immune sensing. Transcriptome analysis of DENV-infected human monocyte-derived dendritic cells (Mo-DC) revealed the activation of distinct patterns of gene transcription, with involvement of pathways including the antiviral response, the TNF superfamily and late activation of death receptor signaling. Interestingly, a dominant early gene network associated with the Nrf2-dependent antioxidant response was also identified; DENV infection induced an early production of ROS that was dependent on NADPH-oxidase, and was essential for the activation of inflammatory and antiviral programs, through NF-κB and IRF-3 transcription factors, respectively. Using a high throughput qPCR assay, we demonstrated that interfering with NADPH-oxidase inhibited DENV-induced antiviral and inflammatory responses. We also demonstrated that the antioxidant pathway controlled by the transcription factor Nrf2 is a pivotal upstream link to the regulation of DENV-induced antiviral and inflammatory responses under oxidative conditions. In conclusion, these findings demonstrate that ROS production is crucial for effective activation of pathways leading to innate immune responses against DENV infection in human Mo-DC. Nichols, Carmen oth He, Zhong oth Hiscott, John oth Enthalten in Elsevier McLaughlin, Richard J. ELSEVIER The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types 2022 the official journal of the International Cytokine Society Oxford [u.a.] (DE-627)ELV008219540 volume:63 year:2013 number:3 pages:287 https://doi.org/10.1016/j.cyto.2013.06.191 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.83 Rheumatologie Orthopädie VZ AR 63 2013 3 287 045F 570 |
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The rapid host response to virus infection is crucial for establishment of the antiviral state and for the release of pro-inflammatory mediators that coordinate the adaptive immune response. Induction of antiviral and inflammatory genes is achieved largely through recognition of viral nucleic acid motifs by pattern recognition receptors. Dengue virus (DENV) is a significant human pathogen that causes a wide spectrum of clinical symptoms, ranging from mild dengue fever to severe hemorrhagic fever and shock syndrome. The cytosolic receptors RIG-I/MDA5 as well as the membrane-bound TLR3/TLR7 localized in the endosomes are important sensors of DENV infection. The role of reactive oxygen species (ROS) in the activation of biological processes such as autophagy, necrosis, and inflammasome activation adds another layer of complexity to the regulation of immune sensing. Transcriptome analysis of DENV-infected human monocyte-derived dendritic cells (Mo-DC) revealed the activation of distinct patterns of gene transcription, with involvement of pathways including the antiviral response, the TNF superfamily and late activation of death receptor signaling. Interestingly, a dominant early gene network associated with the Nrf2-dependent antioxidant response was also identified; DENV infection induced an early production of ROS that was dependent on NADPH-oxidase, and was essential for the activation of inflammatory and antiviral programs, through NF-κB and IRF-3 transcription factors, respectively. Using a high throughput qPCR assay, we demonstrated that interfering with NADPH-oxidase inhibited DENV-induced antiviral and inflammatory responses. We also demonstrated that the antioxidant pathway controlled by the transcription factor Nrf2 is a pivotal upstream link to the regulation of DENV-induced antiviral and inflammatory responses under oxidative conditions. In conclusion, these findings demonstrate that ROS production is crucial for effective activation of pathways leading to innate immune responses against DENV infection in human Mo-DC. |
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The rapid host response to virus infection is crucial for establishment of the antiviral state and for the release of pro-inflammatory mediators that coordinate the adaptive immune response. Induction of antiviral and inflammatory genes is achieved largely through recognition of viral nucleic acid motifs by pattern recognition receptors. Dengue virus (DENV) is a significant human pathogen that causes a wide spectrum of clinical symptoms, ranging from mild dengue fever to severe hemorrhagic fever and shock syndrome. The cytosolic receptors RIG-I/MDA5 as well as the membrane-bound TLR3/TLR7 localized in the endosomes are important sensors of DENV infection. The role of reactive oxygen species (ROS) in the activation of biological processes such as autophagy, necrosis, and inflammasome activation adds another layer of complexity to the regulation of immune sensing. Transcriptome analysis of DENV-infected human monocyte-derived dendritic cells (Mo-DC) revealed the activation of distinct patterns of gene transcription, with involvement of pathways including the antiviral response, the TNF superfamily and late activation of death receptor signaling. Interestingly, a dominant early gene network associated with the Nrf2-dependent antioxidant response was also identified; DENV infection induced an early production of ROS that was dependent on NADPH-oxidase, and was essential for the activation of inflammatory and antiviral programs, through NF-κB and IRF-3 transcription factors, respectively. Using a high throughput qPCR assay, we demonstrated that interfering with NADPH-oxidase inhibited DENV-induced antiviral and inflammatory responses. We also demonstrated that the antioxidant pathway controlled by the transcription factor Nrf2 is a pivotal upstream link to the regulation of DENV-induced antiviral and inflammatory responses under oxidative conditions. In conclusion, these findings demonstrate that ROS production is crucial for effective activation of pathways leading to innate immune responses against DENV infection in human Mo-DC. |
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