Type I interferon in the pathogenesis of systemic lupus erythematosus
• Type I IFN is implicated in SLE pathogenesis by multiple lines of evidence, including genetics and induction of SLE by IFN treatment. • Nucleic-acid sensing pathways influence the threshold of activation and triggering of type I IFN production. • Abnormalities in extracellular processing of DNA ca...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Postal, Mariana [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2020 |
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| Umfang: |
8 |
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| Übergeordnetes Werk: |
Enthalten in: Formulation of antiretroviral nanocrystals and development into a microneedle delivery system for potential treatment of HIV-associated neurocognitive disorder (HAND) - Abbate, Marco T.A. ELSEVIER, 2023, Philadelphia, Pa |
|---|---|
| Übergeordnetes Werk: |
volume:67 ; year:2020 ; pages:87-94 ; extent:8 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.coi.2020.10.014 |
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| 520 | |a • Type I IFN is implicated in SLE pathogenesis by multiple lines of evidence, including genetics and induction of SLE by IFN treatment. • Nucleic-acid sensing pathways influence the threshold of activation and triggering of type I IFN production. • Abnormalities in extracellular processing of DNA can enhance type I IFN production. • High type I IFN levels are associated with nephritis, mucocutaneous manifestations, and the presence of autoantibodies in SLE. • Anifrolumab, a monoclonal antibody that blocks the type I IFN receptor, has shown therapeutic benefit in SLE. | ||
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10.1016/j.coi.2020.10.014 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001251.pica (DE-627)ELV052454207 (ELSEVIER)S0952-7915(20)30114-X DE-627 ger DE-627 rakwb eng 610 VZ 15,3 ssgn PHARM DE-84 fid 44.40 bkl Postal, Mariana verfasserin aut Type I interferon in the pathogenesis of systemic lupus erythematosus 2020 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier • Type I IFN is implicated in SLE pathogenesis by multiple lines of evidence, including genetics and induction of SLE by IFN treatment. • Nucleic-acid sensing pathways influence the threshold of activation and triggering of type I IFN production. • Abnormalities in extracellular processing of DNA can enhance type I IFN production. • High type I IFN levels are associated with nephritis, mucocutaneous manifestations, and the presence of autoantibodies in SLE. • Anifrolumab, a monoclonal antibody that blocks the type I IFN receptor, has shown therapeutic benefit in SLE. Vivaldo, Jessica F oth Fernandez-Ruiz, Ruth oth Paredes, Jacqueline L oth Appenzeller, Simone oth Niewold, Timothy B oth Enthalten in Current Science Abbate, Marco T.A. ELSEVIER Formulation of antiretroviral nanocrystals and development into a microneedle delivery system for potential treatment of HIV-associated neurocognitive disorder (HAND) 2023 Philadelphia, Pa (DE-627)ELV009957871 volume:67 year:2020 pages:87-94 extent:8 https://doi.org/10.1016/j.coi.2020.10.014 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-PHARM SSG-OLC-PHA SSG-OPC-PHA 44.40 Pharmazie Pharmazeutika VZ AR 67 2020 87-94 8 |
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10.1016/j.coi.2020.10.014 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001251.pica (DE-627)ELV052454207 (ELSEVIER)S0952-7915(20)30114-X DE-627 ger DE-627 rakwb eng 610 VZ 15,3 ssgn PHARM DE-84 fid 44.40 bkl Postal, Mariana verfasserin aut Type I interferon in the pathogenesis of systemic lupus erythematosus 2020 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier • Type I IFN is implicated in SLE pathogenesis by multiple lines of evidence, including genetics and induction of SLE by IFN treatment. • Nucleic-acid sensing pathways influence the threshold of activation and triggering of type I IFN production. • Abnormalities in extracellular processing of DNA can enhance type I IFN production. • High type I IFN levels are associated with nephritis, mucocutaneous manifestations, and the presence of autoantibodies in SLE. • Anifrolumab, a monoclonal antibody that blocks the type I IFN receptor, has shown therapeutic benefit in SLE. Vivaldo, Jessica F oth Fernandez-Ruiz, Ruth oth Paredes, Jacqueline L oth Appenzeller, Simone oth Niewold, Timothy B oth Enthalten in Current Science Abbate, Marco T.A. ELSEVIER Formulation of antiretroviral nanocrystals and development into a microneedle delivery system for potential treatment of HIV-associated neurocognitive disorder (HAND) 2023 Philadelphia, Pa (DE-627)ELV009957871 volume:67 year:2020 pages:87-94 extent:8 https://doi.org/10.1016/j.coi.2020.10.014 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-PHARM SSG-OLC-PHA SSG-OPC-PHA 44.40 Pharmazie Pharmazeutika VZ AR 67 2020 87-94 8 |
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10.1016/j.coi.2020.10.014 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001251.pica (DE-627)ELV052454207 (ELSEVIER)S0952-7915(20)30114-X DE-627 ger DE-627 rakwb eng 610 VZ 15,3 ssgn PHARM DE-84 fid 44.40 bkl Postal, Mariana verfasserin aut Type I interferon in the pathogenesis of systemic lupus erythematosus 2020 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier • Type I IFN is implicated in SLE pathogenesis by multiple lines of evidence, including genetics and induction of SLE by IFN treatment. • Nucleic-acid sensing pathways influence the threshold of activation and triggering of type I IFN production. • Abnormalities in extracellular processing of DNA can enhance type I IFN production. • High type I IFN levels are associated with nephritis, mucocutaneous manifestations, and the presence of autoantibodies in SLE. • Anifrolumab, a monoclonal antibody that blocks the type I IFN receptor, has shown therapeutic benefit in SLE. Vivaldo, Jessica F oth Fernandez-Ruiz, Ruth oth Paredes, Jacqueline L oth Appenzeller, Simone oth Niewold, Timothy B oth Enthalten in Current Science Abbate, Marco T.A. ELSEVIER Formulation of antiretroviral nanocrystals and development into a microneedle delivery system for potential treatment of HIV-associated neurocognitive disorder (HAND) 2023 Philadelphia, Pa (DE-627)ELV009957871 volume:67 year:2020 pages:87-94 extent:8 https://doi.org/10.1016/j.coi.2020.10.014 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-PHARM SSG-OLC-PHA SSG-OPC-PHA 44.40 Pharmazie Pharmazeutika VZ AR 67 2020 87-94 8 |
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10.1016/j.coi.2020.10.014 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001251.pica (DE-627)ELV052454207 (ELSEVIER)S0952-7915(20)30114-X DE-627 ger DE-627 rakwb eng 610 VZ 15,3 ssgn PHARM DE-84 fid 44.40 bkl Postal, Mariana verfasserin aut Type I interferon in the pathogenesis of systemic lupus erythematosus 2020 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier • Type I IFN is implicated in SLE pathogenesis by multiple lines of evidence, including genetics and induction of SLE by IFN treatment. • Nucleic-acid sensing pathways influence the threshold of activation and triggering of type I IFN production. • Abnormalities in extracellular processing of DNA can enhance type I IFN production. • High type I IFN levels are associated with nephritis, mucocutaneous manifestations, and the presence of autoantibodies in SLE. • Anifrolumab, a monoclonal antibody that blocks the type I IFN receptor, has shown therapeutic benefit in SLE. Vivaldo, Jessica F oth Fernandez-Ruiz, Ruth oth Paredes, Jacqueline L oth Appenzeller, Simone oth Niewold, Timothy B oth Enthalten in Current Science Abbate, Marco T.A. ELSEVIER Formulation of antiretroviral nanocrystals and development into a microneedle delivery system for potential treatment of HIV-associated neurocognitive disorder (HAND) 2023 Philadelphia, Pa (DE-627)ELV009957871 volume:67 year:2020 pages:87-94 extent:8 https://doi.org/10.1016/j.coi.2020.10.014 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-PHARM SSG-OLC-PHA SSG-OPC-PHA 44.40 Pharmazie Pharmazeutika VZ AR 67 2020 87-94 8 |
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Type I interferon in the pathogenesis of systemic lupus erythematosus |
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• Type I IFN is implicated in SLE pathogenesis by multiple lines of evidence, including genetics and induction of SLE by IFN treatment. • Nucleic-acid sensing pathways influence the threshold of activation and triggering of type I IFN production. • Abnormalities in extracellular processing of DNA can enhance type I IFN production. • High type I IFN levels are associated with nephritis, mucocutaneous manifestations, and the presence of autoantibodies in SLE. • Anifrolumab, a monoclonal antibody that blocks the type I IFN receptor, has shown therapeutic benefit in SLE. |
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• Type I IFN is implicated in SLE pathogenesis by multiple lines of evidence, including genetics and induction of SLE by IFN treatment. • Nucleic-acid sensing pathways influence the threshold of activation and triggering of type I IFN production. • Abnormalities in extracellular processing of DNA can enhance type I IFN production. • High type I IFN levels are associated with nephritis, mucocutaneous manifestations, and the presence of autoantibodies in SLE. • Anifrolumab, a monoclonal antibody that blocks the type I IFN receptor, has shown therapeutic benefit in SLE. |
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• Type I IFN is implicated in SLE pathogenesis by multiple lines of evidence, including genetics and induction of SLE by IFN treatment. • Nucleic-acid sensing pathways influence the threshold of activation and triggering of type I IFN production. • Abnormalities in extracellular processing of DNA can enhance type I IFN production. • High type I IFN levels are associated with nephritis, mucocutaneous manifestations, and the presence of autoantibodies in SLE. • Anifrolumab, a monoclonal antibody that blocks the type I IFN receptor, has shown therapeutic benefit in SLE. |
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