Involvement of RORγt-overexpressing T cells in the development of autoimmune arthritis in mice
Differentiation of T helper 17 cells is dependent on the expression of transcription retinoid-related orphan receptor gamma t (RORγt). The purpose of our study is to determine the role of RORγt expression in T cells on the development of collagen-induced arthritis (CIA). CIA was induced in C57BL/6 a...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Kondo, Yuya [verfasserIn] |
|---|
| Format: |
Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2015 |
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| Rechteinformationen: |
Nutzungsrecht: © Kondo et al.; licensee BioMed Central. 2015 |
|---|
| Übergeordnetes Werk: |
Enthalten in: Arthritis research & therapy - London : BioMed Central, 2003, 17(2015), 1, Seite 105 |
|---|---|
| Übergeordnetes Werk: |
volume:17 ; year:2015 ; number:1 ; pages:105 |
| Links: |
|---|
| DOI / URN: |
10.1186/s13075-015-0606-5 |
|---|
| Katalog-ID: |
OLC1961016230 |
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| 245 | 1 | 0 | |a Involvement of RORγt-overexpressing T cells in the development of autoimmune arthritis in mice |
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| 520 | |a Differentiation of T helper 17 cells is dependent on the expression of transcription retinoid-related orphan receptor gamma t (RORγt). The purpose of our study is to determine the role of RORγt expression in T cells on the development of collagen-induced arthritis (CIA). CIA was induced in C57BL/6 and T cell-specific RORγt transgenic (RORγt Tg) mice. At day 10 post-1st-immunization, lymph node (LN) cells were cultured with type II collagen (CII), and the expression levels of various cytokines and transcription factors on CD4+ T cells were measured. Total cells or CD4+ cells of draining LN were harvested from each mouse group after CII-immunization and transferred into C57BL/6 mice, and then CIA was induced in recipient mice. The expression levels of RORγt and other surface antigens, and the production of cytokines were analyzed in forkhead box P3 (Foxp3)+ regulatory T (Treg) cells. Foxp3+ Treg cells were analyzed for suppressive activity against proliferation of effector CD4+ T cells. Interlukin (IL)-10 neutralizing antibody was administrated in the course of CIA. CIA was significantly suppressed in RORγt Tg mice compared with C57BL/6 mice. RORγt expression and IL-17 production were significantly higher in CII-reactive CD4+ T cells from RORγt Tg mice. Arthritis was significantly attenuated in C57BL/6 mice recipient of cells from RORγt Tg mice. Most of Foxp3+ Treg cells expressed RORγt, produced IL-10 but not IL-17, and overexpressed CC chemokine receptor 6 (CCR6) and surface antigens related to the suppressive activity of Foxp3+ Treg cells in RORγt Tg mice. In vitro suppression assay demonstrated significant augmentation of the suppressive capacity of Foxp3+ Treg cells in RORγt Tg mice. CIA was exacerbated in both C57BL/6 mice and RORγt Tg mice by the treatment of anti-IL-10 antibody. Our results indicated that RORγt overexpression in T cells protected against the development of CIA. The protective effects were mediated, at least in part, through the anti-inflammatory effects including high production of IL-10 of RORγt+Foxp3+ Treg cells. | ||
| 540 | |a Nutzungsrecht: © Kondo et al.; licensee BioMed Central. 2015 | ||
| 650 | 4 | |a Arthritis, Experimental - metabolism | |
| 650 | 4 | |a Arthritis, Experimental - genetics | |
| 650 | 4 | |a RNA - genetics | |
| 650 | 4 | |a Nuclear Receptor Subfamily 1, Group F, Member 3 - genetics | |
| 650 | 4 | |a Arthritis, Experimental - immunology | |
| 650 | 4 | |a T-Lymphocytes, Regulatory - immunology | |
| 650 | 4 | |a Autoimmune Diseases - immunology | |
| 650 | 4 | |a Autoimmune Diseases - metabolism | |
| 650 | 4 | |a Nuclear Receptor Subfamily 1, Group F, Member 3 - biosynthesis | |
| 650 | 4 | |a Autoimmune Diseases - genetics | |
| 700 | 1 | |a Yao, Zhaojin |4 oth | |
| 700 | 1 | |a Tahara, Masahiro |4 oth | |
| 700 | 1 | |a Iizuka, Mana |4 oth | |
| 700 | 1 | |a Yokosawa, Masahiro |4 oth | |
| 700 | 1 | |a Kaneko, Shunta |4 oth | |
| 700 | 1 | |a Segawa, Seiji |4 oth | |
| 700 | 1 | |a Tsuboi, Hiroto |4 oth | |
| 700 | 1 | |a Yoh, Keigyou |4 oth | |
| 700 | 1 | |a Takahashi, Satoru |4 oth | |
| 700 | 1 | |a Matsumoto, Isao |4 oth | |
| 700 | 1 | |a Sumida, Takayuki |4 oth | |
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10.1186/s13075-015-0606-5 doi PQ20160430 (DE-627)OLC1961016230 (DE-599)GBVOLC1961016230 (PRQ)c1801-6cf9f0e418d83321a76251f8e776a86143453a32dc5f270f2ce5642eea202ea83 (KEY)0427448220150000017000100105involvementofrortoverexpressingtcellsinthedevelopm DE-627 ger DE-627 rakwb eng 610 DNB Kondo, Yuya verfasserin aut Involvement of RORγt-overexpressing T cells in the development of autoimmune arthritis in mice 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Differentiation of T helper 17 cells is dependent on the expression of transcription retinoid-related orphan receptor gamma t (RORγt). The purpose of our study is to determine the role of RORγt expression in T cells on the development of collagen-induced arthritis (CIA). CIA was induced in C57BL/6 and T cell-specific RORγt transgenic (RORγt Tg) mice. At day 10 post-1st-immunization, lymph node (LN) cells were cultured with type II collagen (CII), and the expression levels of various cytokines and transcription factors on CD4+ T cells were measured. Total cells or CD4+ cells of draining LN were harvested from each mouse group after CII-immunization and transferred into C57BL/6 mice, and then CIA was induced in recipient mice. The expression levels of RORγt and other surface antigens, and the production of cytokines were analyzed in forkhead box P3 (Foxp3)+ regulatory T (Treg) cells. Foxp3+ Treg cells were analyzed for suppressive activity against proliferation of effector CD4+ T cells. Interlukin (IL)-10 neutralizing antibody was administrated in the course of CIA. CIA was significantly suppressed in RORγt Tg mice compared with C57BL/6 mice. RORγt expression and IL-17 production were significantly higher in CII-reactive CD4+ T cells from RORγt Tg mice. Arthritis was significantly attenuated in C57BL/6 mice recipient of cells from RORγt Tg mice. Most of Foxp3+ Treg cells expressed RORγt, produced IL-10 but not IL-17, and overexpressed CC chemokine receptor 6 (CCR6) and surface antigens related to the suppressive activity of Foxp3+ Treg cells in RORγt Tg mice. In vitro suppression assay demonstrated significant augmentation of the suppressive capacity of Foxp3+ Treg cells in RORγt Tg mice. CIA was exacerbated in both C57BL/6 mice and RORγt Tg mice by the treatment of anti-IL-10 antibody. Our results indicated that RORγt overexpression in T cells protected against the development of CIA. The protective effects were mediated, at least in part, through the anti-inflammatory effects including high production of IL-10 of RORγt+Foxp3+ Treg cells. Nutzungsrecht: © Kondo et al.; licensee BioMed Central. 2015 Arthritis, Experimental - metabolism Arthritis, Experimental - genetics RNA - genetics Nuclear Receptor Subfamily 1, Group F, Member 3 - genetics Arthritis, Experimental - immunology T-Lymphocytes, Regulatory - immunology Autoimmune Diseases - immunology Autoimmune Diseases - metabolism Nuclear Receptor Subfamily 1, Group F, Member 3 - biosynthesis Autoimmune Diseases - genetics Yao, Zhaojin oth Tahara, Masahiro oth Iizuka, Mana oth Yokosawa, Masahiro oth Kaneko, Shunta oth Segawa, Seiji oth Tsuboi, Hiroto oth Yoh, Keigyou oth Takahashi, Satoru oth Matsumoto, Isao oth Sumida, Takayuki oth Enthalten in Arthritis research & therapy London : BioMed Central, 2003 17(2015), 1, Seite 105 (DE-627)363765530 (DE-600)2107602-9 (DE-576)379407604 1478-6354 nnns volume:17 year:2015 number:1 pages:105 http://dx.doi.org/10.1186/s13075-015-0606-5 Volltext http://www.ncbi.nlm.nih.gov/pubmed/25928901 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4436146&tool=pmcentrez&rendertype=abstract GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-NED SSG-OLC-PHA SSG-OLC-DE-84 AR 17 2015 1 105 |
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10.1186/s13075-015-0606-5 doi PQ20160430 (DE-627)OLC1961016230 (DE-599)GBVOLC1961016230 (PRQ)c1801-6cf9f0e418d83321a76251f8e776a86143453a32dc5f270f2ce5642eea202ea83 (KEY)0427448220150000017000100105involvementofrortoverexpressingtcellsinthedevelopm DE-627 ger DE-627 rakwb eng 610 DNB Kondo, Yuya verfasserin aut Involvement of RORγt-overexpressing T cells in the development of autoimmune arthritis in mice 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Differentiation of T helper 17 cells is dependent on the expression of transcription retinoid-related orphan receptor gamma t (RORγt). The purpose of our study is to determine the role of RORγt expression in T cells on the development of collagen-induced arthritis (CIA). CIA was induced in C57BL/6 and T cell-specific RORγt transgenic (RORγt Tg) mice. At day 10 post-1st-immunization, lymph node (LN) cells were cultured with type II collagen (CII), and the expression levels of various cytokines and transcription factors on CD4+ T cells were measured. Total cells or CD4+ cells of draining LN were harvested from each mouse group after CII-immunization and transferred into C57BL/6 mice, and then CIA was induced in recipient mice. The expression levels of RORγt and other surface antigens, and the production of cytokines were analyzed in forkhead box P3 (Foxp3)+ regulatory T (Treg) cells. Foxp3+ Treg cells were analyzed for suppressive activity against proliferation of effector CD4+ T cells. Interlukin (IL)-10 neutralizing antibody was administrated in the course of CIA. CIA was significantly suppressed in RORγt Tg mice compared with C57BL/6 mice. RORγt expression and IL-17 production were significantly higher in CII-reactive CD4+ T cells from RORγt Tg mice. Arthritis was significantly attenuated in C57BL/6 mice recipient of cells from RORγt Tg mice. Most of Foxp3+ Treg cells expressed RORγt, produced IL-10 but not IL-17, and overexpressed CC chemokine receptor 6 (CCR6) and surface antigens related to the suppressive activity of Foxp3+ Treg cells in RORγt Tg mice. In vitro suppression assay demonstrated significant augmentation of the suppressive capacity of Foxp3+ Treg cells in RORγt Tg mice. CIA was exacerbated in both C57BL/6 mice and RORγt Tg mice by the treatment of anti-IL-10 antibody. Our results indicated that RORγt overexpression in T cells protected against the development of CIA. The protective effects were mediated, at least in part, through the anti-inflammatory effects including high production of IL-10 of RORγt+Foxp3+ Treg cells. Nutzungsrecht: © Kondo et al.; licensee BioMed Central. 2015 Arthritis, Experimental - metabolism Arthritis, Experimental - genetics RNA - genetics Nuclear Receptor Subfamily 1, Group F, Member 3 - genetics Arthritis, Experimental - immunology T-Lymphocytes, Regulatory - immunology Autoimmune Diseases - immunology Autoimmune Diseases - metabolism Nuclear Receptor Subfamily 1, Group F, Member 3 - biosynthesis Autoimmune Diseases - genetics Yao, Zhaojin oth Tahara, Masahiro oth Iizuka, Mana oth Yokosawa, Masahiro oth Kaneko, Shunta oth Segawa, Seiji oth Tsuboi, Hiroto oth Yoh, Keigyou oth Takahashi, Satoru oth Matsumoto, Isao oth Sumida, Takayuki oth Enthalten in Arthritis research & therapy London : BioMed Central, 2003 17(2015), 1, Seite 105 (DE-627)363765530 (DE-600)2107602-9 (DE-576)379407604 1478-6354 nnns volume:17 year:2015 number:1 pages:105 http://dx.doi.org/10.1186/s13075-015-0606-5 Volltext http://www.ncbi.nlm.nih.gov/pubmed/25928901 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4436146&tool=pmcentrez&rendertype=abstract GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-NED SSG-OLC-PHA SSG-OLC-DE-84 AR 17 2015 1 105 |
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10.1186/s13075-015-0606-5 doi PQ20160430 (DE-627)OLC1961016230 (DE-599)GBVOLC1961016230 (PRQ)c1801-6cf9f0e418d83321a76251f8e776a86143453a32dc5f270f2ce5642eea202ea83 (KEY)0427448220150000017000100105involvementofrortoverexpressingtcellsinthedevelopm DE-627 ger DE-627 rakwb eng 610 DNB Kondo, Yuya verfasserin aut Involvement of RORγt-overexpressing T cells in the development of autoimmune arthritis in mice 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Differentiation of T helper 17 cells is dependent on the expression of transcription retinoid-related orphan receptor gamma t (RORγt). The purpose of our study is to determine the role of RORγt expression in T cells on the development of collagen-induced arthritis (CIA). CIA was induced in C57BL/6 and T cell-specific RORγt transgenic (RORγt Tg) mice. At day 10 post-1st-immunization, lymph node (LN) cells were cultured with type II collagen (CII), and the expression levels of various cytokines and transcription factors on CD4+ T cells were measured. Total cells or CD4+ cells of draining LN were harvested from each mouse group after CII-immunization and transferred into C57BL/6 mice, and then CIA was induced in recipient mice. The expression levels of RORγt and other surface antigens, and the production of cytokines were analyzed in forkhead box P3 (Foxp3)+ regulatory T (Treg) cells. Foxp3+ Treg cells were analyzed for suppressive activity against proliferation of effector CD4+ T cells. Interlukin (IL)-10 neutralizing antibody was administrated in the course of CIA. CIA was significantly suppressed in RORγt Tg mice compared with C57BL/6 mice. RORγt expression and IL-17 production were significantly higher in CII-reactive CD4+ T cells from RORγt Tg mice. Arthritis was significantly attenuated in C57BL/6 mice recipient of cells from RORγt Tg mice. Most of Foxp3+ Treg cells expressed RORγt, produced IL-10 but not IL-17, and overexpressed CC chemokine receptor 6 (CCR6) and surface antigens related to the suppressive activity of Foxp3+ Treg cells in RORγt Tg mice. In vitro suppression assay demonstrated significant augmentation of the suppressive capacity of Foxp3+ Treg cells in RORγt Tg mice. CIA was exacerbated in both C57BL/6 mice and RORγt Tg mice by the treatment of anti-IL-10 antibody. Our results indicated that RORγt overexpression in T cells protected against the development of CIA. The protective effects were mediated, at least in part, through the anti-inflammatory effects including high production of IL-10 of RORγt+Foxp3+ Treg cells. Nutzungsrecht: © Kondo et al.; licensee BioMed Central. 2015 Arthritis, Experimental - metabolism Arthritis, Experimental - genetics RNA - genetics Nuclear Receptor Subfamily 1, Group F, Member 3 - genetics Arthritis, Experimental - immunology T-Lymphocytes, Regulatory - immunology Autoimmune Diseases - immunology Autoimmune Diseases - metabolism Nuclear Receptor Subfamily 1, Group F, Member 3 - biosynthesis Autoimmune Diseases - genetics Yao, Zhaojin oth Tahara, Masahiro oth Iizuka, Mana oth Yokosawa, Masahiro oth Kaneko, Shunta oth Segawa, Seiji oth Tsuboi, Hiroto oth Yoh, Keigyou oth Takahashi, Satoru oth Matsumoto, Isao oth Sumida, Takayuki oth Enthalten in Arthritis research & therapy London : BioMed Central, 2003 17(2015), 1, Seite 105 (DE-627)363765530 (DE-600)2107602-9 (DE-576)379407604 1478-6354 nnns volume:17 year:2015 number:1 pages:105 http://dx.doi.org/10.1186/s13075-015-0606-5 Volltext http://www.ncbi.nlm.nih.gov/pubmed/25928901 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4436146&tool=pmcentrez&rendertype=abstract GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-NED SSG-OLC-PHA SSG-OLC-DE-84 AR 17 2015 1 105 |
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10.1186/s13075-015-0606-5 doi PQ20160430 (DE-627)OLC1961016230 (DE-599)GBVOLC1961016230 (PRQ)c1801-6cf9f0e418d83321a76251f8e776a86143453a32dc5f270f2ce5642eea202ea83 (KEY)0427448220150000017000100105involvementofrortoverexpressingtcellsinthedevelopm DE-627 ger DE-627 rakwb eng 610 DNB Kondo, Yuya verfasserin aut Involvement of RORγt-overexpressing T cells in the development of autoimmune arthritis in mice 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Differentiation of T helper 17 cells is dependent on the expression of transcription retinoid-related orphan receptor gamma t (RORγt). The purpose of our study is to determine the role of RORγt expression in T cells on the development of collagen-induced arthritis (CIA). CIA was induced in C57BL/6 and T cell-specific RORγt transgenic (RORγt Tg) mice. At day 10 post-1st-immunization, lymph node (LN) cells were cultured with type II collagen (CII), and the expression levels of various cytokines and transcription factors on CD4+ T cells were measured. Total cells or CD4+ cells of draining LN were harvested from each mouse group after CII-immunization and transferred into C57BL/6 mice, and then CIA was induced in recipient mice. The expression levels of RORγt and other surface antigens, and the production of cytokines were analyzed in forkhead box P3 (Foxp3)+ regulatory T (Treg) cells. Foxp3+ Treg cells were analyzed for suppressive activity against proliferation of effector CD4+ T cells. Interlukin (IL)-10 neutralizing antibody was administrated in the course of CIA. CIA was significantly suppressed in RORγt Tg mice compared with C57BL/6 mice. RORγt expression and IL-17 production were significantly higher in CII-reactive CD4+ T cells from RORγt Tg mice. Arthritis was significantly attenuated in C57BL/6 mice recipient of cells from RORγt Tg mice. Most of Foxp3+ Treg cells expressed RORγt, produced IL-10 but not IL-17, and overexpressed CC chemokine receptor 6 (CCR6) and surface antigens related to the suppressive activity of Foxp3+ Treg cells in RORγt Tg mice. In vitro suppression assay demonstrated significant augmentation of the suppressive capacity of Foxp3+ Treg cells in RORγt Tg mice. CIA was exacerbated in both C57BL/6 mice and RORγt Tg mice by the treatment of anti-IL-10 antibody. Our results indicated that RORγt overexpression in T cells protected against the development of CIA. The protective effects were mediated, at least in part, through the anti-inflammatory effects including high production of IL-10 of RORγt+Foxp3+ Treg cells. Nutzungsrecht: © Kondo et al.; licensee BioMed Central. 2015 Arthritis, Experimental - metabolism Arthritis, Experimental - genetics RNA - genetics Nuclear Receptor Subfamily 1, Group F, Member 3 - genetics Arthritis, Experimental - immunology T-Lymphocytes, Regulatory - immunology Autoimmune Diseases - immunology Autoimmune Diseases - metabolism Nuclear Receptor Subfamily 1, Group F, Member 3 - biosynthesis Autoimmune Diseases - genetics Yao, Zhaojin oth Tahara, Masahiro oth Iizuka, Mana oth Yokosawa, Masahiro oth Kaneko, Shunta oth Segawa, Seiji oth Tsuboi, Hiroto oth Yoh, Keigyou oth Takahashi, Satoru oth Matsumoto, Isao oth Sumida, Takayuki oth Enthalten in Arthritis research & therapy London : BioMed Central, 2003 17(2015), 1, Seite 105 (DE-627)363765530 (DE-600)2107602-9 (DE-576)379407604 1478-6354 nnns volume:17 year:2015 number:1 pages:105 http://dx.doi.org/10.1186/s13075-015-0606-5 Volltext http://www.ncbi.nlm.nih.gov/pubmed/25928901 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4436146&tool=pmcentrez&rendertype=abstract GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-NED SSG-OLC-PHA SSG-OLC-DE-84 AR 17 2015 1 105 |
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10.1186/s13075-015-0606-5 doi PQ20160430 (DE-627)OLC1961016230 (DE-599)GBVOLC1961016230 (PRQ)c1801-6cf9f0e418d83321a76251f8e776a86143453a32dc5f270f2ce5642eea202ea83 (KEY)0427448220150000017000100105involvementofrortoverexpressingtcellsinthedevelopm DE-627 ger DE-627 rakwb eng 610 DNB Kondo, Yuya verfasserin aut Involvement of RORγt-overexpressing T cells in the development of autoimmune arthritis in mice 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Differentiation of T helper 17 cells is dependent on the expression of transcription retinoid-related orphan receptor gamma t (RORγt). The purpose of our study is to determine the role of RORγt expression in T cells on the development of collagen-induced arthritis (CIA). CIA was induced in C57BL/6 and T cell-specific RORγt transgenic (RORγt Tg) mice. At day 10 post-1st-immunization, lymph node (LN) cells were cultured with type II collagen (CII), and the expression levels of various cytokines and transcription factors on CD4+ T cells were measured. Total cells or CD4+ cells of draining LN were harvested from each mouse group after CII-immunization and transferred into C57BL/6 mice, and then CIA was induced in recipient mice. The expression levels of RORγt and other surface antigens, and the production of cytokines were analyzed in forkhead box P3 (Foxp3)+ regulatory T (Treg) cells. Foxp3+ Treg cells were analyzed for suppressive activity against proliferation of effector CD4+ T cells. Interlukin (IL)-10 neutralizing antibody was administrated in the course of CIA. CIA was significantly suppressed in RORγt Tg mice compared with C57BL/6 mice. RORγt expression and IL-17 production were significantly higher in CII-reactive CD4+ T cells from RORγt Tg mice. Arthritis was significantly attenuated in C57BL/6 mice recipient of cells from RORγt Tg mice. Most of Foxp3+ Treg cells expressed RORγt, produced IL-10 but not IL-17, and overexpressed CC chemokine receptor 6 (CCR6) and surface antigens related to the suppressive activity of Foxp3+ Treg cells in RORγt Tg mice. In vitro suppression assay demonstrated significant augmentation of the suppressive capacity of Foxp3+ Treg cells in RORγt Tg mice. CIA was exacerbated in both C57BL/6 mice and RORγt Tg mice by the treatment of anti-IL-10 antibody. Our results indicated that RORγt overexpression in T cells protected against the development of CIA. The protective effects were mediated, at least in part, through the anti-inflammatory effects including high production of IL-10 of RORγt+Foxp3+ Treg cells. Nutzungsrecht: © Kondo et al.; licensee BioMed Central. 2015 Arthritis, Experimental - metabolism Arthritis, Experimental - genetics RNA - genetics Nuclear Receptor Subfamily 1, Group F, Member 3 - genetics Arthritis, Experimental - immunology T-Lymphocytes, Regulatory - immunology Autoimmune Diseases - immunology Autoimmune Diseases - metabolism Nuclear Receptor Subfamily 1, Group F, Member 3 - biosynthesis Autoimmune Diseases - genetics Yao, Zhaojin oth Tahara, Masahiro oth Iizuka, Mana oth Yokosawa, Masahiro oth Kaneko, Shunta oth Segawa, Seiji oth Tsuboi, Hiroto oth Yoh, Keigyou oth Takahashi, Satoru oth Matsumoto, Isao oth Sumida, Takayuki oth Enthalten in Arthritis research & therapy London : BioMed Central, 2003 17(2015), 1, Seite 105 (DE-627)363765530 (DE-600)2107602-9 (DE-576)379407604 1478-6354 nnns volume:17 year:2015 number:1 pages:105 http://dx.doi.org/10.1186/s13075-015-0606-5 Volltext http://www.ncbi.nlm.nih.gov/pubmed/25928901 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4436146&tool=pmcentrez&rendertype=abstract GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-NED SSG-OLC-PHA SSG-OLC-DE-84 AR 17 2015 1 105 |
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involvement of rorγt-overexpressing t cells in the development of autoimmune arthritis in mice |
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Involvement of RORγt-overexpressing T cells in the development of autoimmune arthritis in mice |
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Differentiation of T helper 17 cells is dependent on the expression of transcription retinoid-related orphan receptor gamma t (RORγt). The purpose of our study is to determine the role of RORγt expression in T cells on the development of collagen-induced arthritis (CIA). CIA was induced in C57BL/6 and T cell-specific RORγt transgenic (RORγt Tg) mice. At day 10 post-1st-immunization, lymph node (LN) cells were cultured with type II collagen (CII), and the expression levels of various cytokines and transcription factors on CD4+ T cells were measured. Total cells or CD4+ cells of draining LN were harvested from each mouse group after CII-immunization and transferred into C57BL/6 mice, and then CIA was induced in recipient mice. The expression levels of RORγt and other surface antigens, and the production of cytokines were analyzed in forkhead box P3 (Foxp3)+ regulatory T (Treg) cells. Foxp3+ Treg cells were analyzed for suppressive activity against proliferation of effector CD4+ T cells. Interlukin (IL)-10 neutralizing antibody was administrated in the course of CIA. CIA was significantly suppressed in RORγt Tg mice compared with C57BL/6 mice. RORγt expression and IL-17 production were significantly higher in CII-reactive CD4+ T cells from RORγt Tg mice. Arthritis was significantly attenuated in C57BL/6 mice recipient of cells from RORγt Tg mice. Most of Foxp3+ Treg cells expressed RORγt, produced IL-10 but not IL-17, and overexpressed CC chemokine receptor 6 (CCR6) and surface antigens related to the suppressive activity of Foxp3+ Treg cells in RORγt Tg mice. In vitro suppression assay demonstrated significant augmentation of the suppressive capacity of Foxp3+ Treg cells in RORγt Tg mice. CIA was exacerbated in both C57BL/6 mice and RORγt Tg mice by the treatment of anti-IL-10 antibody. Our results indicated that RORγt overexpression in T cells protected against the development of CIA. The protective effects were mediated, at least in part, through the anti-inflammatory effects including high production of IL-10 of RORγt+Foxp3+ Treg cells. |
| abstractGer |
Differentiation of T helper 17 cells is dependent on the expression of transcription retinoid-related orphan receptor gamma t (RORγt). The purpose of our study is to determine the role of RORγt expression in T cells on the development of collagen-induced arthritis (CIA). CIA was induced in C57BL/6 and T cell-specific RORγt transgenic (RORγt Tg) mice. At day 10 post-1st-immunization, lymph node (LN) cells were cultured with type II collagen (CII), and the expression levels of various cytokines and transcription factors on CD4+ T cells were measured. Total cells or CD4+ cells of draining LN were harvested from each mouse group after CII-immunization and transferred into C57BL/6 mice, and then CIA was induced in recipient mice. The expression levels of RORγt and other surface antigens, and the production of cytokines were analyzed in forkhead box P3 (Foxp3)+ regulatory T (Treg) cells. Foxp3+ Treg cells were analyzed for suppressive activity against proliferation of effector CD4+ T cells. Interlukin (IL)-10 neutralizing antibody was administrated in the course of CIA. CIA was significantly suppressed in RORγt Tg mice compared with C57BL/6 mice. RORγt expression and IL-17 production were significantly higher in CII-reactive CD4+ T cells from RORγt Tg mice. Arthritis was significantly attenuated in C57BL/6 mice recipient of cells from RORγt Tg mice. Most of Foxp3+ Treg cells expressed RORγt, produced IL-10 but not IL-17, and overexpressed CC chemokine receptor 6 (CCR6) and surface antigens related to the suppressive activity of Foxp3+ Treg cells in RORγt Tg mice. In vitro suppression assay demonstrated significant augmentation of the suppressive capacity of Foxp3+ Treg cells in RORγt Tg mice. CIA was exacerbated in both C57BL/6 mice and RORγt Tg mice by the treatment of anti-IL-10 antibody. Our results indicated that RORγt overexpression in T cells protected against the development of CIA. The protective effects were mediated, at least in part, through the anti-inflammatory effects including high production of IL-10 of RORγt+Foxp3+ Treg cells. |
| abstract_unstemmed |
Differentiation of T helper 17 cells is dependent on the expression of transcription retinoid-related orphan receptor gamma t (RORγt). The purpose of our study is to determine the role of RORγt expression in T cells on the development of collagen-induced arthritis (CIA). CIA was induced in C57BL/6 and T cell-specific RORγt transgenic (RORγt Tg) mice. At day 10 post-1st-immunization, lymph node (LN) cells were cultured with type II collagen (CII), and the expression levels of various cytokines and transcription factors on CD4+ T cells were measured. Total cells or CD4+ cells of draining LN were harvested from each mouse group after CII-immunization and transferred into C57BL/6 mice, and then CIA was induced in recipient mice. The expression levels of RORγt and other surface antigens, and the production of cytokines were analyzed in forkhead box P3 (Foxp3)+ regulatory T (Treg) cells. Foxp3+ Treg cells were analyzed for suppressive activity against proliferation of effector CD4+ T cells. Interlukin (IL)-10 neutralizing antibody was administrated in the course of CIA. CIA was significantly suppressed in RORγt Tg mice compared with C57BL/6 mice. RORγt expression and IL-17 production were significantly higher in CII-reactive CD4+ T cells from RORγt Tg mice. Arthritis was significantly attenuated in C57BL/6 mice recipient of cells from RORγt Tg mice. Most of Foxp3+ Treg cells expressed RORγt, produced IL-10 but not IL-17, and overexpressed CC chemokine receptor 6 (CCR6) and surface antigens related to the suppressive activity of Foxp3+ Treg cells in RORγt Tg mice. In vitro suppression assay demonstrated significant augmentation of the suppressive capacity of Foxp3+ Treg cells in RORγt Tg mice. CIA was exacerbated in both C57BL/6 mice and RORγt Tg mice by the treatment of anti-IL-10 antibody. Our results indicated that RORγt overexpression in T cells protected against the development of CIA. The protective effects were mediated, at least in part, through the anti-inflammatory effects including high production of IL-10 of RORγt+Foxp3+ Treg cells. |
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The purpose of our study is to determine the role of RORγt expression in T cells on the development of collagen-induced arthritis (CIA). CIA was induced in C57BL/6 and T cell-specific RORγt transgenic (RORγt Tg) mice. At day 10 post-1st-immunization, lymph node (LN) cells were cultured with type II collagen (CII), and the expression levels of various cytokines and transcription factors on CD4+ T cells were measured. Total cells or CD4+ cells of draining LN were harvested from each mouse group after CII-immunization and transferred into C57BL/6 mice, and then CIA was induced in recipient mice. The expression levels of RORγt and other surface antigens, and the production of cytokines were analyzed in forkhead box P3 (Foxp3)+ regulatory T (Treg) cells. Foxp3+ Treg cells were analyzed for suppressive activity against proliferation of effector CD4+ T cells. Interlukin (IL)-10 neutralizing antibody was administrated in the course of CIA. CIA was significantly suppressed in RORγt Tg mice compared with C57BL/6 mice. RORγt expression and IL-17 production were significantly higher in CII-reactive CD4+ T cells from RORγt Tg mice. Arthritis was significantly attenuated in C57BL/6 mice recipient of cells from RORγt Tg mice. Most of Foxp3+ Treg cells expressed RORγt, produced IL-10 but not IL-17, and overexpressed CC chemokine receptor 6 (CCR6) and surface antigens related to the suppressive activity of Foxp3+ Treg cells in RORγt Tg mice. In vitro suppression assay demonstrated significant augmentation of the suppressive capacity of Foxp3+ Treg cells in RORγt Tg mice. CIA was exacerbated in both C57BL/6 mice and RORγt Tg mice by the treatment of anti-IL-10 antibody. Our results indicated that RORγt overexpression in T cells protected against the development of CIA. The protective effects were mediated, at least in part, through the anti-inflammatory effects including high production of IL-10 of RORγt+Foxp3+ Treg cells.</subfield></datafield><datafield tag="540" ind1=" " ind2=" "><subfield code="a">Nutzungsrecht: © Kondo et al.; licensee BioMed Central. 2015</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Arthritis, Experimental - metabolism</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Arthritis, Experimental - genetics</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">RNA - genetics</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Nuclear Receptor Subfamily 1, Group F, Member 3 - genetics</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Arthritis, Experimental - immunology</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">T-Lymphocytes, Regulatory - immunology</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Autoimmune Diseases - immunology</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Autoimmune Diseases - metabolism</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Nuclear Receptor Subfamily 1, Group F, Member 3 - biosynthesis</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Autoimmune Diseases - genetics</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yao, Zhaojin</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Tahara, Masahiro</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Iizuka, Mana</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yokosawa, Masahiro</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kaneko, Shunta</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Segawa, Seiji</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Tsuboi, Hiroto</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yoh, Keigyou</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Takahashi, Satoru</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Matsumoto, Isao</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Sumida, Takayuki</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Arthritis research & therapy</subfield><subfield code="d">London : BioMed Central, 2003</subfield><subfield code="g">17(2015), 1, Seite 105</subfield><subfield code="w">(DE-627)363765530</subfield><subfield code="w">(DE-600)2107602-9</subfield><subfield code="w">(DE-576)379407604</subfield><subfield code="x">1478-6354</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:17</subfield><subfield code="g">year:2015</subfield><subfield code="g">number:1</subfield><subfield code="g">pages:105</subfield></datafield><datafield tag="856" ind1="4" ind2="1"><subfield code="u">http://dx.doi.org/10.1186/s13075-015-0606-5</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">http://www.ncbi.nlm.nih.gov/pubmed/25928901</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4436146&tool=pmcentrez&rendertype=abstract</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_OLC</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-NED</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-DE-84</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">17</subfield><subfield code="j">2015</subfield><subfield code="e">1</subfield><subfield code="h">105</subfield></datafield></record></collection>
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