MicroRNA-183 and microRNA-96 are associated with autoimmune responses by regulating T cell activation
MircoRNAs (miRs) are small molecules that regulate gene expression at the posttranscriptional level. They have been proposed to be involved in the regulation of several immune responses including autoimmunity. Here, we identified miR-183 and miR-96 to be highly expressed in CD4+ T cells from periphe...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Thiel, Jacqueline [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2019transfer abstract |
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| Schlagwörter: |
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| Umfang: |
10 |
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| Übergeordnetes Werk: |
Enthalten in: Influence of the wind farm integration on load flow and voltage in electrical power system - imen, Labed ELSEVIER, 2016, London |
|---|---|
| Übergeordnetes Werk: |
volume:96 ; year:2019 ; pages:94-103 ; extent:10 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.jaut.2018.08.010 |
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| 245 | 1 | 0 | |a MicroRNA-183 and microRNA-96 are associated with autoimmune responses by regulating T cell activation |
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| 520 | |a MircoRNAs (miRs) are small molecules that regulate gene expression at the posttranscriptional level. They have been proposed to be involved in the regulation of several immune responses including autoimmunity. Here, we identified miR-183 and miR-96 to be highly expressed in CD4+ T cells from peripheral blood of Graves' orbitopathy (GO) patients as well as in human and murine T cells upon activation in vitro. By using Luciferase-based binding assays, we identified EGR-1 as target for miR-183 and miR-96. Overexpression of miR-183 and miR-96 in murine CD4+ T cells by retroviral gene transfer resulted in decreased EGR-1 and PTEN expression, elevated Akt phosphorylation and enhanced proliferation. In contrast, treatment of murine CD4+ T cells with specific antagomiRs increased EGR-1 and PTEN expression and interfered with the proliferative activity upon stimulation in vitro. Strikingly, adoptive transfer of miR-183 and miR-96 overexpressing antigen-specific T cells into INS-HA/Rag2KO mice accelerated the development of autoimmune diabetes, whereas transfer of antagomiR-treated cells delayed the disease onset. These results indicate that miR-183 and miR-96 have the ability to regulate the strength of T cell activation and thereby the development and severity of T cell-dependent autoimmune diseases. | ||
| 520 | |a MircoRNAs (miRs) are small molecules that regulate gene expression at the posttranscriptional level. They have been proposed to be involved in the regulation of several immune responses including autoimmunity. Here, we identified miR-183 and miR-96 to be highly expressed in CD4+ T cells from peripheral blood of Graves' orbitopathy (GO) patients as well as in human and murine T cells upon activation in vitro. By using Luciferase-based binding assays, we identified EGR-1 as target for miR-183 and miR-96. Overexpression of miR-183 and miR-96 in murine CD4+ T cells by retroviral gene transfer resulted in decreased EGR-1 and PTEN expression, elevated Akt phosphorylation and enhanced proliferation. In contrast, treatment of murine CD4+ T cells with specific antagomiRs increased EGR-1 and PTEN expression and interfered with the proliferative activity upon stimulation in vitro. Strikingly, adoptive transfer of miR-183 and miR-96 overexpressing antigen-specific T cells into INS-HA/Rag2KO mice accelerated the development of autoimmune diabetes, whereas transfer of antagomiR-treated cells delayed the disease onset. These results indicate that miR-183 and miR-96 have the ability to regulate the strength of T cell activation and thereby the development and severity of T cell-dependent autoimmune diseases. | ||
| 650 | 7 | |a Autoimmunity |2 Elsevier | |
| 650 | 7 | |a microRNA-183 |2 Elsevier | |
| 650 | 7 | |a Immune regulation |2 Elsevier | |
| 650 | 7 | |a T cells |2 Elsevier | |
| 650 | 7 | |a microRNA-96 |2 Elsevier | |
| 700 | 1 | |a Alter, Christina |4 oth | |
| 700 | 1 | |a Luppus, Sina |4 oth | |
| 700 | 1 | |a Eckstein, Anja |4 oth | |
| 700 | 1 | |a Tan, Susanne |4 oth | |
| 700 | 1 | |a Führer, Dagmar |4 oth | |
| 700 | 1 | |a Pastille, Eva |4 oth | |
| 700 | 1 | |a Westendorf, Astrid M. |4 oth | |
| 700 | 1 | |a Buer, Jan |4 oth | |
| 700 | 1 | |a Hansen, Wiebke |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Academic Press |a imen, Labed ELSEVIER |t Influence of the wind farm integration on load flow and voltage in electrical power system |d 2016 |g London |w (DE-627)ELV014127067 |
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10.1016/j.jaut.2018.08.010 doi GBV00000000000512.pica (DE-627)ELV045280983 (ELSEVIER)S0896-8411(18)30302-0 DE-627 ger DE-627 rakwb eng 660 VZ 620 VZ 610 VZ 44.94 bkl Thiel, Jacqueline verfasserin aut MicroRNA-183 and microRNA-96 are associated with autoimmune responses by regulating T cell activation 2019transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier MircoRNAs (miRs) are small molecules that regulate gene expression at the posttranscriptional level. They have been proposed to be involved in the regulation of several immune responses including autoimmunity. Here, we identified miR-183 and miR-96 to be highly expressed in CD4+ T cells from peripheral blood of Graves' orbitopathy (GO) patients as well as in human and murine T cells upon activation in vitro. By using Luciferase-based binding assays, we identified EGR-1 as target for miR-183 and miR-96. Overexpression of miR-183 and miR-96 in murine CD4+ T cells by retroviral gene transfer resulted in decreased EGR-1 and PTEN expression, elevated Akt phosphorylation and enhanced proliferation. In contrast, treatment of murine CD4+ T cells with specific antagomiRs increased EGR-1 and PTEN expression and interfered with the proliferative activity upon stimulation in vitro. Strikingly, adoptive transfer of miR-183 and miR-96 overexpressing antigen-specific T cells into INS-HA/Rag2KO mice accelerated the development of autoimmune diabetes, whereas transfer of antagomiR-treated cells delayed the disease onset. These results indicate that miR-183 and miR-96 have the ability to regulate the strength of T cell activation and thereby the development and severity of T cell-dependent autoimmune diseases. MircoRNAs (miRs) are small molecules that regulate gene expression at the posttranscriptional level. They have been proposed to be involved in the regulation of several immune responses including autoimmunity. Here, we identified miR-183 and miR-96 to be highly expressed in CD4+ T cells from peripheral blood of Graves' orbitopathy (GO) patients as well as in human and murine T cells upon activation in vitro. By using Luciferase-based binding assays, we identified EGR-1 as target for miR-183 and miR-96. Overexpression of miR-183 and miR-96 in murine CD4+ T cells by retroviral gene transfer resulted in decreased EGR-1 and PTEN expression, elevated Akt phosphorylation and enhanced proliferation. In contrast, treatment of murine CD4+ T cells with specific antagomiRs increased EGR-1 and PTEN expression and interfered with the proliferative activity upon stimulation in vitro. Strikingly, adoptive transfer of miR-183 and miR-96 overexpressing antigen-specific T cells into INS-HA/Rag2KO mice accelerated the development of autoimmune diabetes, whereas transfer of antagomiR-treated cells delayed the disease onset. These results indicate that miR-183 and miR-96 have the ability to regulate the strength of T cell activation and thereby the development and severity of T cell-dependent autoimmune diseases. Autoimmunity Elsevier microRNA-183 Elsevier Immune regulation Elsevier T cells Elsevier microRNA-96 Elsevier Alter, Christina oth Luppus, Sina oth Eckstein, Anja oth Tan, Susanne oth Führer, Dagmar oth Pastille, Eva oth Westendorf, Astrid M. oth Buer, Jan oth Hansen, Wiebke oth Enthalten in Academic Press imen, Labed ELSEVIER Influence of the wind farm integration on load flow and voltage in electrical power system 2016 London (DE-627)ELV014127067 volume:96 year:2019 pages:94-103 extent:10 https://doi.org/10.1016/j.jaut.2018.08.010 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.94 Hals-Nasen-Ohrenheilkunde VZ AR 96 2019 94-103 10 |
| spelling |
10.1016/j.jaut.2018.08.010 doi GBV00000000000512.pica (DE-627)ELV045280983 (ELSEVIER)S0896-8411(18)30302-0 DE-627 ger DE-627 rakwb eng 660 VZ 620 VZ 610 VZ 44.94 bkl Thiel, Jacqueline verfasserin aut MicroRNA-183 and microRNA-96 are associated with autoimmune responses by regulating T cell activation 2019transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier MircoRNAs (miRs) are small molecules that regulate gene expression at the posttranscriptional level. They have been proposed to be involved in the regulation of several immune responses including autoimmunity. Here, we identified miR-183 and miR-96 to be highly expressed in CD4+ T cells from peripheral blood of Graves' orbitopathy (GO) patients as well as in human and murine T cells upon activation in vitro. By using Luciferase-based binding assays, we identified EGR-1 as target for miR-183 and miR-96. Overexpression of miR-183 and miR-96 in murine CD4+ T cells by retroviral gene transfer resulted in decreased EGR-1 and PTEN expression, elevated Akt phosphorylation and enhanced proliferation. In contrast, treatment of murine CD4+ T cells with specific antagomiRs increased EGR-1 and PTEN expression and interfered with the proliferative activity upon stimulation in vitro. Strikingly, adoptive transfer of miR-183 and miR-96 overexpressing antigen-specific T cells into INS-HA/Rag2KO mice accelerated the development of autoimmune diabetes, whereas transfer of antagomiR-treated cells delayed the disease onset. These results indicate that miR-183 and miR-96 have the ability to regulate the strength of T cell activation and thereby the development and severity of T cell-dependent autoimmune diseases. MircoRNAs (miRs) are small molecules that regulate gene expression at the posttranscriptional level. They have been proposed to be involved in the regulation of several immune responses including autoimmunity. Here, we identified miR-183 and miR-96 to be highly expressed in CD4+ T cells from peripheral blood of Graves' orbitopathy (GO) patients as well as in human and murine T cells upon activation in vitro. By using Luciferase-based binding assays, we identified EGR-1 as target for miR-183 and miR-96. Overexpression of miR-183 and miR-96 in murine CD4+ T cells by retroviral gene transfer resulted in decreased EGR-1 and PTEN expression, elevated Akt phosphorylation and enhanced proliferation. In contrast, treatment of murine CD4+ T cells with specific antagomiRs increased EGR-1 and PTEN expression and interfered with the proliferative activity upon stimulation in vitro. Strikingly, adoptive transfer of miR-183 and miR-96 overexpressing antigen-specific T cells into INS-HA/Rag2KO mice accelerated the development of autoimmune diabetes, whereas transfer of antagomiR-treated cells delayed the disease onset. These results indicate that miR-183 and miR-96 have the ability to regulate the strength of T cell activation and thereby the development and severity of T cell-dependent autoimmune diseases. Autoimmunity Elsevier microRNA-183 Elsevier Immune regulation Elsevier T cells Elsevier microRNA-96 Elsevier Alter, Christina oth Luppus, Sina oth Eckstein, Anja oth Tan, Susanne oth Führer, Dagmar oth Pastille, Eva oth Westendorf, Astrid M. oth Buer, Jan oth Hansen, Wiebke oth Enthalten in Academic Press imen, Labed ELSEVIER Influence of the wind farm integration on load flow and voltage in electrical power system 2016 London (DE-627)ELV014127067 volume:96 year:2019 pages:94-103 extent:10 https://doi.org/10.1016/j.jaut.2018.08.010 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.94 Hals-Nasen-Ohrenheilkunde VZ AR 96 2019 94-103 10 |
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10.1016/j.jaut.2018.08.010 doi GBV00000000000512.pica (DE-627)ELV045280983 (ELSEVIER)S0896-8411(18)30302-0 DE-627 ger DE-627 rakwb eng 660 VZ 620 VZ 610 VZ 44.94 bkl Thiel, Jacqueline verfasserin aut MicroRNA-183 and microRNA-96 are associated with autoimmune responses by regulating T cell activation 2019transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier MircoRNAs (miRs) are small molecules that regulate gene expression at the posttranscriptional level. They have been proposed to be involved in the regulation of several immune responses including autoimmunity. Here, we identified miR-183 and miR-96 to be highly expressed in CD4+ T cells from peripheral blood of Graves' orbitopathy (GO) patients as well as in human and murine T cells upon activation in vitro. By using Luciferase-based binding assays, we identified EGR-1 as target for miR-183 and miR-96. Overexpression of miR-183 and miR-96 in murine CD4+ T cells by retroviral gene transfer resulted in decreased EGR-1 and PTEN expression, elevated Akt phosphorylation and enhanced proliferation. In contrast, treatment of murine CD4+ T cells with specific antagomiRs increased EGR-1 and PTEN expression and interfered with the proliferative activity upon stimulation in vitro. Strikingly, adoptive transfer of miR-183 and miR-96 overexpressing antigen-specific T cells into INS-HA/Rag2KO mice accelerated the development of autoimmune diabetes, whereas transfer of antagomiR-treated cells delayed the disease onset. These results indicate that miR-183 and miR-96 have the ability to regulate the strength of T cell activation and thereby the development and severity of T cell-dependent autoimmune diseases. MircoRNAs (miRs) are small molecules that regulate gene expression at the posttranscriptional level. They have been proposed to be involved in the regulation of several immune responses including autoimmunity. Here, we identified miR-183 and miR-96 to be highly expressed in CD4+ T cells from peripheral blood of Graves' orbitopathy (GO) patients as well as in human and murine T cells upon activation in vitro. By using Luciferase-based binding assays, we identified EGR-1 as target for miR-183 and miR-96. Overexpression of miR-183 and miR-96 in murine CD4+ T cells by retroviral gene transfer resulted in decreased EGR-1 and PTEN expression, elevated Akt phosphorylation and enhanced proliferation. In contrast, treatment of murine CD4+ T cells with specific antagomiRs increased EGR-1 and PTEN expression and interfered with the proliferative activity upon stimulation in vitro. Strikingly, adoptive transfer of miR-183 and miR-96 overexpressing antigen-specific T cells into INS-HA/Rag2KO mice accelerated the development of autoimmune diabetes, whereas transfer of antagomiR-treated cells delayed the disease onset. These results indicate that miR-183 and miR-96 have the ability to regulate the strength of T cell activation and thereby the development and severity of T cell-dependent autoimmune diseases. Autoimmunity Elsevier microRNA-183 Elsevier Immune regulation Elsevier T cells Elsevier microRNA-96 Elsevier Alter, Christina oth Luppus, Sina oth Eckstein, Anja oth Tan, Susanne oth Führer, Dagmar oth Pastille, Eva oth Westendorf, Astrid M. oth Buer, Jan oth Hansen, Wiebke oth Enthalten in Academic Press imen, Labed ELSEVIER Influence of the wind farm integration on load flow and voltage in electrical power system 2016 London (DE-627)ELV014127067 volume:96 year:2019 pages:94-103 extent:10 https://doi.org/10.1016/j.jaut.2018.08.010 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.94 Hals-Nasen-Ohrenheilkunde VZ AR 96 2019 94-103 10 |
| allfieldsGer |
10.1016/j.jaut.2018.08.010 doi GBV00000000000512.pica (DE-627)ELV045280983 (ELSEVIER)S0896-8411(18)30302-0 DE-627 ger DE-627 rakwb eng 660 VZ 620 VZ 610 VZ 44.94 bkl Thiel, Jacqueline verfasserin aut MicroRNA-183 and microRNA-96 are associated with autoimmune responses by regulating T cell activation 2019transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier MircoRNAs (miRs) are small molecules that regulate gene expression at the posttranscriptional level. They have been proposed to be involved in the regulation of several immune responses including autoimmunity. Here, we identified miR-183 and miR-96 to be highly expressed in CD4+ T cells from peripheral blood of Graves' orbitopathy (GO) patients as well as in human and murine T cells upon activation in vitro. By using Luciferase-based binding assays, we identified EGR-1 as target for miR-183 and miR-96. Overexpression of miR-183 and miR-96 in murine CD4+ T cells by retroviral gene transfer resulted in decreased EGR-1 and PTEN expression, elevated Akt phosphorylation and enhanced proliferation. In contrast, treatment of murine CD4+ T cells with specific antagomiRs increased EGR-1 and PTEN expression and interfered with the proliferative activity upon stimulation in vitro. Strikingly, adoptive transfer of miR-183 and miR-96 overexpressing antigen-specific T cells into INS-HA/Rag2KO mice accelerated the development of autoimmune diabetes, whereas transfer of antagomiR-treated cells delayed the disease onset. These results indicate that miR-183 and miR-96 have the ability to regulate the strength of T cell activation and thereby the development and severity of T cell-dependent autoimmune diseases. MircoRNAs (miRs) are small molecules that regulate gene expression at the posttranscriptional level. They have been proposed to be involved in the regulation of several immune responses including autoimmunity. Here, we identified miR-183 and miR-96 to be highly expressed in CD4+ T cells from peripheral blood of Graves' orbitopathy (GO) patients as well as in human and murine T cells upon activation in vitro. By using Luciferase-based binding assays, we identified EGR-1 as target for miR-183 and miR-96. Overexpression of miR-183 and miR-96 in murine CD4+ T cells by retroviral gene transfer resulted in decreased EGR-1 and PTEN expression, elevated Akt phosphorylation and enhanced proliferation. In contrast, treatment of murine CD4+ T cells with specific antagomiRs increased EGR-1 and PTEN expression and interfered with the proliferative activity upon stimulation in vitro. Strikingly, adoptive transfer of miR-183 and miR-96 overexpressing antigen-specific T cells into INS-HA/Rag2KO mice accelerated the development of autoimmune diabetes, whereas transfer of antagomiR-treated cells delayed the disease onset. These results indicate that miR-183 and miR-96 have the ability to regulate the strength of T cell activation and thereby the development and severity of T cell-dependent autoimmune diseases. Autoimmunity Elsevier microRNA-183 Elsevier Immune regulation Elsevier T cells Elsevier microRNA-96 Elsevier Alter, Christina oth Luppus, Sina oth Eckstein, Anja oth Tan, Susanne oth Führer, Dagmar oth Pastille, Eva oth Westendorf, Astrid M. oth Buer, Jan oth Hansen, Wiebke oth Enthalten in Academic Press imen, Labed ELSEVIER Influence of the wind farm integration on load flow and voltage in electrical power system 2016 London (DE-627)ELV014127067 volume:96 year:2019 pages:94-103 extent:10 https://doi.org/10.1016/j.jaut.2018.08.010 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.94 Hals-Nasen-Ohrenheilkunde VZ AR 96 2019 94-103 10 |
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10.1016/j.jaut.2018.08.010 doi GBV00000000000512.pica (DE-627)ELV045280983 (ELSEVIER)S0896-8411(18)30302-0 DE-627 ger DE-627 rakwb eng 660 VZ 620 VZ 610 VZ 44.94 bkl Thiel, Jacqueline verfasserin aut MicroRNA-183 and microRNA-96 are associated with autoimmune responses by regulating T cell activation 2019transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier MircoRNAs (miRs) are small molecules that regulate gene expression at the posttranscriptional level. They have been proposed to be involved in the regulation of several immune responses including autoimmunity. Here, we identified miR-183 and miR-96 to be highly expressed in CD4+ T cells from peripheral blood of Graves' orbitopathy (GO) patients as well as in human and murine T cells upon activation in vitro. By using Luciferase-based binding assays, we identified EGR-1 as target for miR-183 and miR-96. Overexpression of miR-183 and miR-96 in murine CD4+ T cells by retroviral gene transfer resulted in decreased EGR-1 and PTEN expression, elevated Akt phosphorylation and enhanced proliferation. In contrast, treatment of murine CD4+ T cells with specific antagomiRs increased EGR-1 and PTEN expression and interfered with the proliferative activity upon stimulation in vitro. Strikingly, adoptive transfer of miR-183 and miR-96 overexpressing antigen-specific T cells into INS-HA/Rag2KO mice accelerated the development of autoimmune diabetes, whereas transfer of antagomiR-treated cells delayed the disease onset. These results indicate that miR-183 and miR-96 have the ability to regulate the strength of T cell activation and thereby the development and severity of T cell-dependent autoimmune diseases. MircoRNAs (miRs) are small molecules that regulate gene expression at the posttranscriptional level. They have been proposed to be involved in the regulation of several immune responses including autoimmunity. Here, we identified miR-183 and miR-96 to be highly expressed in CD4+ T cells from peripheral blood of Graves' orbitopathy (GO) patients as well as in human and murine T cells upon activation in vitro. By using Luciferase-based binding assays, we identified EGR-1 as target for miR-183 and miR-96. Overexpression of miR-183 and miR-96 in murine CD4+ T cells by retroviral gene transfer resulted in decreased EGR-1 and PTEN expression, elevated Akt phosphorylation and enhanced proliferation. In contrast, treatment of murine CD4+ T cells with specific antagomiRs increased EGR-1 and PTEN expression and interfered with the proliferative activity upon stimulation in vitro. Strikingly, adoptive transfer of miR-183 and miR-96 overexpressing antigen-specific T cells into INS-HA/Rag2KO mice accelerated the development of autoimmune diabetes, whereas transfer of antagomiR-treated cells delayed the disease onset. These results indicate that miR-183 and miR-96 have the ability to regulate the strength of T cell activation and thereby the development and severity of T cell-dependent autoimmune diseases. Autoimmunity Elsevier microRNA-183 Elsevier Immune regulation Elsevier T cells Elsevier microRNA-96 Elsevier Alter, Christina oth Luppus, Sina oth Eckstein, Anja oth Tan, Susanne oth Führer, Dagmar oth Pastille, Eva oth Westendorf, Astrid M. oth Buer, Jan oth Hansen, Wiebke oth Enthalten in Academic Press imen, Labed ELSEVIER Influence of the wind farm integration on load flow and voltage in electrical power system 2016 London (DE-627)ELV014127067 volume:96 year:2019 pages:94-103 extent:10 https://doi.org/10.1016/j.jaut.2018.08.010 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.94 Hals-Nasen-Ohrenheilkunde VZ AR 96 2019 94-103 10 |
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Thiel, Jacqueline @@aut@@ Alter, Christina @@oth@@ Luppus, Sina @@oth@@ Eckstein, Anja @@oth@@ Tan, Susanne @@oth@@ Führer, Dagmar @@oth@@ Pastille, Eva @@oth@@ Westendorf, Astrid M. @@oth@@ Buer, Jan @@oth@@ Hansen, Wiebke @@oth@@ |
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microrna-183 and microrna-96 are associated with autoimmune responses by regulating t cell activation |
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MicroRNA-183 and microRNA-96 are associated with autoimmune responses by regulating T cell activation |
| abstract |
MircoRNAs (miRs) are small molecules that regulate gene expression at the posttranscriptional level. They have been proposed to be involved in the regulation of several immune responses including autoimmunity. Here, we identified miR-183 and miR-96 to be highly expressed in CD4+ T cells from peripheral blood of Graves' orbitopathy (GO) patients as well as in human and murine T cells upon activation in vitro. By using Luciferase-based binding assays, we identified EGR-1 as target for miR-183 and miR-96. Overexpression of miR-183 and miR-96 in murine CD4+ T cells by retroviral gene transfer resulted in decreased EGR-1 and PTEN expression, elevated Akt phosphorylation and enhanced proliferation. In contrast, treatment of murine CD4+ T cells with specific antagomiRs increased EGR-1 and PTEN expression and interfered with the proliferative activity upon stimulation in vitro. Strikingly, adoptive transfer of miR-183 and miR-96 overexpressing antigen-specific T cells into INS-HA/Rag2KO mice accelerated the development of autoimmune diabetes, whereas transfer of antagomiR-treated cells delayed the disease onset. These results indicate that miR-183 and miR-96 have the ability to regulate the strength of T cell activation and thereby the development and severity of T cell-dependent autoimmune diseases. |
| abstractGer |
MircoRNAs (miRs) are small molecules that regulate gene expression at the posttranscriptional level. They have been proposed to be involved in the regulation of several immune responses including autoimmunity. Here, we identified miR-183 and miR-96 to be highly expressed in CD4+ T cells from peripheral blood of Graves' orbitopathy (GO) patients as well as in human and murine T cells upon activation in vitro. By using Luciferase-based binding assays, we identified EGR-1 as target for miR-183 and miR-96. Overexpression of miR-183 and miR-96 in murine CD4+ T cells by retroviral gene transfer resulted in decreased EGR-1 and PTEN expression, elevated Akt phosphorylation and enhanced proliferation. In contrast, treatment of murine CD4+ T cells with specific antagomiRs increased EGR-1 and PTEN expression and interfered with the proliferative activity upon stimulation in vitro. Strikingly, adoptive transfer of miR-183 and miR-96 overexpressing antigen-specific T cells into INS-HA/Rag2KO mice accelerated the development of autoimmune diabetes, whereas transfer of antagomiR-treated cells delayed the disease onset. These results indicate that miR-183 and miR-96 have the ability to regulate the strength of T cell activation and thereby the development and severity of T cell-dependent autoimmune diseases. |
| abstract_unstemmed |
MircoRNAs (miRs) are small molecules that regulate gene expression at the posttranscriptional level. They have been proposed to be involved in the regulation of several immune responses including autoimmunity. Here, we identified miR-183 and miR-96 to be highly expressed in CD4+ T cells from peripheral blood of Graves' orbitopathy (GO) patients as well as in human and murine T cells upon activation in vitro. By using Luciferase-based binding assays, we identified EGR-1 as target for miR-183 and miR-96. Overexpression of miR-183 and miR-96 in murine CD4+ T cells by retroviral gene transfer resulted in decreased EGR-1 and PTEN expression, elevated Akt phosphorylation and enhanced proliferation. In contrast, treatment of murine CD4+ T cells with specific antagomiRs increased EGR-1 and PTEN expression and interfered with the proliferative activity upon stimulation in vitro. Strikingly, adoptive transfer of miR-183 and miR-96 overexpressing antigen-specific T cells into INS-HA/Rag2KO mice accelerated the development of autoimmune diabetes, whereas transfer of antagomiR-treated cells delayed the disease onset. These results indicate that miR-183 and miR-96 have the ability to regulate the strength of T cell activation and thereby the development and severity of T cell-dependent autoimmune diseases. |
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