Long noncoding RNA derived from CD244 signaling epigenetically controls CD8+ T-cell immune responses in tuberculosis infection
Molecular mechanisms for T-cell immune responses modulated by T cell-inhibitory molecules during tuberculosis (TB) infection remain unclear. Here, we show that active human TB infection up-regulates CD244 and CD244 signaling-associated molecules in CD8(+) T cells and that blockade of CD244 signaling...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Dan Huang [verfasserIn] |
|---|
| Format: |
Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2015 |
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| Übergeordnetes Werk: |
Enthalten in: Proceedings of the National Academy of Sciences of the United States of America - Washington, DC : NAS, 1877, 112(2015), 29, Seite E3883-E3892 |
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| Übergeordnetes Werk: |
volume:112 ; year:2015 ; number:29 ; pages:E3883-E3892 |
| Links: |
|---|
| DOI / URN: |
10.1073/pnas.1501662112 |
|---|
| Katalog-ID: |
OLC1970275596 |
|---|
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| 245 | 1 | 0 | |a Long noncoding RNA derived from CD244 signaling epigenetically controls CD8+ T-cell immune responses in tuberculosis infection |
| 264 | 1 | |c 2015 | |
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| 520 | |a Molecular mechanisms for T-cell immune responses modulated by T cell-inhibitory molecules during tuberculosis (TB) infection remain unclear. Here, we show that active human TB infection up-regulates CD244 and CD244 signaling-associated molecules in CD8(+) T cells and that blockade of CD244 signaling enhances production of IFN-γ and TNF-α. CD244 expression/signaling in TB correlates with high levels of a long noncoding RNA (lncRNA)-BC050410 [named as lncRNA-AS-GSTT1(1-72) or lncRNA-CD244] in the CD244(+)CD8(+) T-cell subpopulation. CD244 signaling drives lncRNA-CD244 expression via sustaining a permissive chromatin state in the lncRNA-CD244 locus. By recruiting polycomb protein enhancer of zeste homolog 2 (EZH2) to infg/tnfa promoters, lncRNA-CD244 mediates H3K27 trimethylation at infg/tnfa loci toward repressive chromatin states and inhibits IFN-γ/TNF-α expression in CD8(+) T cells. Such inhibition can be reversed by knock down of lncRNA-CD244. Interestingly, adoptive transfer of lncRNA-CD244-depressed CD8(+) T cells to Mycobacterium tuberculosis (MTB)-infected mice reduced MTB infection and TB pathology compared with lncRNA-CD244-expressed controls. Thus, this work uncovers previously unidentified mechanisms in which T cell-inhibitory signaling and lncRNAs regulate T-cell responses and host defense against TB infection. | ||
| 650 | 4 | |a Interferon-gamma - biosynthesis | |
| 650 | 4 | |a Polycomb Repressive Complex 2 - metabolism | |
| 650 | 4 | |a Promoter Regions, Genetic - genetics | |
| 650 | 4 | |a Protein Binding - drug effects | |
| 650 | 4 | |a Interferon-gamma - genetics | |
| 650 | 4 | |a CD8-Positive T-Lymphocytes - immunology | |
| 650 | 4 | |a Tumor Necrosis Factor-alpha - genetics | |
| 650 | 4 | |a RNA, Long Noncoding - genetics | |
| 650 | 4 | |a Tuberculosis - immunology | |
| 650 | 4 | |a Chromatin - metabolism | |
| 650 | 4 | |a Intracellular Signaling Peptides and Proteins - metabolism | |
| 650 | 4 | |a Apoptosis - genetics | |
| 650 | 4 | |a CD8-Positive T-Lymphocytes - cytology | |
| 650 | 4 | |a Up-Regulation - drug effects | |
| 650 | 4 | |a Tumor Necrosis Factor-alpha - biosynthesis | |
| 650 | 4 | |a Apoptosis - drug effects | |
| 650 | 4 | |a Signal Transduction - drug effects | |
| 650 | 4 | |a Immunity - drug effects | |
| 650 | 4 | |a Antibodies, Monoclonal - pharmacology | |
| 650 | 4 | |a Signal Transduction - genetics | |
| 650 | 4 | |a Transcription Factors - metabolism | |
| 650 | 4 | |a Immunity - genetics | |
| 650 | 4 | |a CD8-Positive T-Lymphocytes - drug effects | |
| 650 | 4 | |a Epigenesis, Genetic - drug effects | |
| 650 | 4 | |a Bacteria | |
| 650 | 4 | |a Chromatin | |
| 650 | 4 | |a Tuberculosis | |
| 650 | 4 | |a Correlation analysis | |
| 650 | 4 | |a Molecules | |
| 650 | 4 | |a Rodents | |
| 650 | 4 | |a T cell receptors | |
| 700 | 0 | |a Crystal Y. Chen |4 oth | |
| 700 | 0 | |a Zheng W. Chen |4 oth | |
| 700 | 0 | |a Xiaodan Xie |4 oth | |
| 700 | 0 | |a Yang Wang |4 oth | |
| 700 | 0 | |a Gucheng Zeng |4 oth | |
| 700 | 0 | |a Huiling Zhong |4 oth | |
| 700 | 0 | |a Ling Shen |4 oth | |
| 700 | 0 | |a Hui Zhang |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |t Proceedings of the National Academy of Sciences of the United States of America |d Washington, DC : NAS, 1877 |g 112(2015), 29, Seite E3883-E3892 |w (DE-627)129505269 |w (DE-600)209104-5 |w (DE-576)014909189 |x 0027-8424 |7 nnns |
| 773 | 1 | 8 | |g volume:112 |g year:2015 |g number:29 |g pages:E3883-E3892 |
| 856 | 4 | 1 | |u http://dx.doi.org/10.1073/pnas.1501662112 |3 Volltext |
| 856 | 4 | 2 | |u http://www.pnas.org/content/112/29/E3883.abstract |
| 856 | 4 | 2 | |u http://www.ncbi.nlm.nih.gov/pubmed/26150504 |
| 856 | 4 | 2 | |u http://search.proquest.com/docview/1699087846 |
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10.1073/pnas.1501662112 doi PQ20160211 (DE-627)OLC1970275596 (DE-599)GBVOLC1970275596 (PRQ)c2289-7706fd17485ef0c4e0de2391ee1973f6d620c3e417d5f6449770c6a2a1727e1a3 (KEY)0583363920150000112002903883longnoncodingrnaderivedfromcd244signalingepigeneti DE-627 ger DE-627 rakwb eng 500 DNB 570 AVZ LING fid BIODIV fid Dan Huang verfasserin aut Long noncoding RNA derived from CD244 signaling epigenetically controls CD8+ T-cell immune responses in tuberculosis infection 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Molecular mechanisms for T-cell immune responses modulated by T cell-inhibitory molecules during tuberculosis (TB) infection remain unclear. Here, we show that active human TB infection up-regulates CD244 and CD244 signaling-associated molecules in CD8(+) T cells and that blockade of CD244 signaling enhances production of IFN-γ and TNF-α. CD244 expression/signaling in TB correlates with high levels of a long noncoding RNA (lncRNA)-BC050410 [named as lncRNA-AS-GSTT1(1-72) or lncRNA-CD244] in the CD244(+)CD8(+) T-cell subpopulation. CD244 signaling drives lncRNA-CD244 expression via sustaining a permissive chromatin state in the lncRNA-CD244 locus. By recruiting polycomb protein enhancer of zeste homolog 2 (EZH2) to infg/tnfa promoters, lncRNA-CD244 mediates H3K27 trimethylation at infg/tnfa loci toward repressive chromatin states and inhibits IFN-γ/TNF-α expression in CD8(+) T cells. Such inhibition can be reversed by knock down of lncRNA-CD244. Interestingly, adoptive transfer of lncRNA-CD244-depressed CD8(+) T cells to Mycobacterium tuberculosis (MTB)-infected mice reduced MTB infection and TB pathology compared with lncRNA-CD244-expressed controls. Thus, this work uncovers previously unidentified mechanisms in which T cell-inhibitory signaling and lncRNAs regulate T-cell responses and host defense against TB infection. Interferon-gamma - biosynthesis Polycomb Repressive Complex 2 - metabolism Promoter Regions, Genetic - genetics Protein Binding - drug effects Interferon-gamma - genetics CD8-Positive T-Lymphocytes - immunology Tumor Necrosis Factor-alpha - genetics RNA, Long Noncoding - genetics Tuberculosis - immunology Chromatin - metabolism Intracellular Signaling Peptides and Proteins - metabolism Apoptosis - genetics CD8-Positive T-Lymphocytes - cytology Up-Regulation - drug effects Tumor Necrosis Factor-alpha - biosynthesis Apoptosis - drug effects Signal Transduction - drug effects Immunity - drug effects Antibodies, Monoclonal - pharmacology Signal Transduction - genetics Transcription Factors - metabolism Immunity - genetics CD8-Positive T-Lymphocytes - drug effects Epigenesis, Genetic - drug effects Bacteria Chromatin Tuberculosis Correlation analysis Molecules Rodents T cell receptors Crystal Y. Chen oth Zheng W. Chen oth Xiaodan Xie oth Yang Wang oth Gucheng Zeng oth Huiling Zhong oth Ling Shen oth Hui Zhang oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 112(2015), 29, Seite E3883-E3892 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:112 year:2015 number:29 pages:E3883-E3892 http://dx.doi.org/10.1073/pnas.1501662112 Volltext http://www.pnas.org/content/112/29/E3883.abstract http://www.ncbi.nlm.nih.gov/pubmed/26150504 http://search.proquest.com/docview/1699087846 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-MAT SSG-OPC-FOR GBV_ILN_40 GBV_ILN_59 AR 112 2015 29 E3883-E3892 |
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10.1073/pnas.1501662112 doi PQ20160211 (DE-627)OLC1970275596 (DE-599)GBVOLC1970275596 (PRQ)c2289-7706fd17485ef0c4e0de2391ee1973f6d620c3e417d5f6449770c6a2a1727e1a3 (KEY)0583363920150000112002903883longnoncodingrnaderivedfromcd244signalingepigeneti DE-627 ger DE-627 rakwb eng 500 DNB 570 AVZ LING fid BIODIV fid Dan Huang verfasserin aut Long noncoding RNA derived from CD244 signaling epigenetically controls CD8+ T-cell immune responses in tuberculosis infection 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Molecular mechanisms for T-cell immune responses modulated by T cell-inhibitory molecules during tuberculosis (TB) infection remain unclear. Here, we show that active human TB infection up-regulates CD244 and CD244 signaling-associated molecules in CD8(+) T cells and that blockade of CD244 signaling enhances production of IFN-γ and TNF-α. CD244 expression/signaling in TB correlates with high levels of a long noncoding RNA (lncRNA)-BC050410 [named as lncRNA-AS-GSTT1(1-72) or lncRNA-CD244] in the CD244(+)CD8(+) T-cell subpopulation. CD244 signaling drives lncRNA-CD244 expression via sustaining a permissive chromatin state in the lncRNA-CD244 locus. By recruiting polycomb protein enhancer of zeste homolog 2 (EZH2) to infg/tnfa promoters, lncRNA-CD244 mediates H3K27 trimethylation at infg/tnfa loci toward repressive chromatin states and inhibits IFN-γ/TNF-α expression in CD8(+) T cells. Such inhibition can be reversed by knock down of lncRNA-CD244. Interestingly, adoptive transfer of lncRNA-CD244-depressed CD8(+) T cells to Mycobacterium tuberculosis (MTB)-infected mice reduced MTB infection and TB pathology compared with lncRNA-CD244-expressed controls. Thus, this work uncovers previously unidentified mechanisms in which T cell-inhibitory signaling and lncRNAs regulate T-cell responses and host defense against TB infection. Interferon-gamma - biosynthesis Polycomb Repressive Complex 2 - metabolism Promoter Regions, Genetic - genetics Protein Binding - drug effects Interferon-gamma - genetics CD8-Positive T-Lymphocytes - immunology Tumor Necrosis Factor-alpha - genetics RNA, Long Noncoding - genetics Tuberculosis - immunology Chromatin - metabolism Intracellular Signaling Peptides and Proteins - metabolism Apoptosis - genetics CD8-Positive T-Lymphocytes - cytology Up-Regulation - drug effects Tumor Necrosis Factor-alpha - biosynthesis Apoptosis - drug effects Signal Transduction - drug effects Immunity - drug effects Antibodies, Monoclonal - pharmacology Signal Transduction - genetics Transcription Factors - metabolism Immunity - genetics CD8-Positive T-Lymphocytes - drug effects Epigenesis, Genetic - drug effects Bacteria Chromatin Tuberculosis Correlation analysis Molecules Rodents T cell receptors Crystal Y. Chen oth Zheng W. Chen oth Xiaodan Xie oth Yang Wang oth Gucheng Zeng oth Huiling Zhong oth Ling Shen oth Hui Zhang oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 112(2015), 29, Seite E3883-E3892 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:112 year:2015 number:29 pages:E3883-E3892 http://dx.doi.org/10.1073/pnas.1501662112 Volltext http://www.pnas.org/content/112/29/E3883.abstract http://www.ncbi.nlm.nih.gov/pubmed/26150504 http://search.proquest.com/docview/1699087846 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-MAT SSG-OPC-FOR GBV_ILN_40 GBV_ILN_59 AR 112 2015 29 E3883-E3892 |
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10.1073/pnas.1501662112 doi PQ20160211 (DE-627)OLC1970275596 (DE-599)GBVOLC1970275596 (PRQ)c2289-7706fd17485ef0c4e0de2391ee1973f6d620c3e417d5f6449770c6a2a1727e1a3 (KEY)0583363920150000112002903883longnoncodingrnaderivedfromcd244signalingepigeneti DE-627 ger DE-627 rakwb eng 500 DNB 570 AVZ LING fid BIODIV fid Dan Huang verfasserin aut Long noncoding RNA derived from CD244 signaling epigenetically controls CD8+ T-cell immune responses in tuberculosis infection 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Molecular mechanisms for T-cell immune responses modulated by T cell-inhibitory molecules during tuberculosis (TB) infection remain unclear. Here, we show that active human TB infection up-regulates CD244 and CD244 signaling-associated molecules in CD8(+) T cells and that blockade of CD244 signaling enhances production of IFN-γ and TNF-α. CD244 expression/signaling in TB correlates with high levels of a long noncoding RNA (lncRNA)-BC050410 [named as lncRNA-AS-GSTT1(1-72) or lncRNA-CD244] in the CD244(+)CD8(+) T-cell subpopulation. CD244 signaling drives lncRNA-CD244 expression via sustaining a permissive chromatin state in the lncRNA-CD244 locus. By recruiting polycomb protein enhancer of zeste homolog 2 (EZH2) to infg/tnfa promoters, lncRNA-CD244 mediates H3K27 trimethylation at infg/tnfa loci toward repressive chromatin states and inhibits IFN-γ/TNF-α expression in CD8(+) T cells. Such inhibition can be reversed by knock down of lncRNA-CD244. Interestingly, adoptive transfer of lncRNA-CD244-depressed CD8(+) T cells to Mycobacterium tuberculosis (MTB)-infected mice reduced MTB infection and TB pathology compared with lncRNA-CD244-expressed controls. Thus, this work uncovers previously unidentified mechanisms in which T cell-inhibitory signaling and lncRNAs regulate T-cell responses and host defense against TB infection. Interferon-gamma - biosynthesis Polycomb Repressive Complex 2 - metabolism Promoter Regions, Genetic - genetics Protein Binding - drug effects Interferon-gamma - genetics CD8-Positive T-Lymphocytes - immunology Tumor Necrosis Factor-alpha - genetics RNA, Long Noncoding - genetics Tuberculosis - immunology Chromatin - metabolism Intracellular Signaling Peptides and Proteins - metabolism Apoptosis - genetics CD8-Positive T-Lymphocytes - cytology Up-Regulation - drug effects Tumor Necrosis Factor-alpha - biosynthesis Apoptosis - drug effects Signal Transduction - drug effects Immunity - drug effects Antibodies, Monoclonal - pharmacology Signal Transduction - genetics Transcription Factors - metabolism Immunity - genetics CD8-Positive T-Lymphocytes - drug effects Epigenesis, Genetic - drug effects Bacteria Chromatin Tuberculosis Correlation analysis Molecules Rodents T cell receptors Crystal Y. Chen oth Zheng W. Chen oth Xiaodan Xie oth Yang Wang oth Gucheng Zeng oth Huiling Zhong oth Ling Shen oth Hui Zhang oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 112(2015), 29, Seite E3883-E3892 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:112 year:2015 number:29 pages:E3883-E3892 http://dx.doi.org/10.1073/pnas.1501662112 Volltext http://www.pnas.org/content/112/29/E3883.abstract http://www.ncbi.nlm.nih.gov/pubmed/26150504 http://search.proquest.com/docview/1699087846 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-MAT SSG-OPC-FOR GBV_ILN_40 GBV_ILN_59 AR 112 2015 29 E3883-E3892 |
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10.1073/pnas.1501662112 doi PQ20160211 (DE-627)OLC1970275596 (DE-599)GBVOLC1970275596 (PRQ)c2289-7706fd17485ef0c4e0de2391ee1973f6d620c3e417d5f6449770c6a2a1727e1a3 (KEY)0583363920150000112002903883longnoncodingrnaderivedfromcd244signalingepigeneti DE-627 ger DE-627 rakwb eng 500 DNB 570 AVZ LING fid BIODIV fid Dan Huang verfasserin aut Long noncoding RNA derived from CD244 signaling epigenetically controls CD8+ T-cell immune responses in tuberculosis infection 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Molecular mechanisms for T-cell immune responses modulated by T cell-inhibitory molecules during tuberculosis (TB) infection remain unclear. Here, we show that active human TB infection up-regulates CD244 and CD244 signaling-associated molecules in CD8(+) T cells and that blockade of CD244 signaling enhances production of IFN-γ and TNF-α. CD244 expression/signaling in TB correlates with high levels of a long noncoding RNA (lncRNA)-BC050410 [named as lncRNA-AS-GSTT1(1-72) or lncRNA-CD244] in the CD244(+)CD8(+) T-cell subpopulation. CD244 signaling drives lncRNA-CD244 expression via sustaining a permissive chromatin state in the lncRNA-CD244 locus. By recruiting polycomb protein enhancer of zeste homolog 2 (EZH2) to infg/tnfa promoters, lncRNA-CD244 mediates H3K27 trimethylation at infg/tnfa loci toward repressive chromatin states and inhibits IFN-γ/TNF-α expression in CD8(+) T cells. Such inhibition can be reversed by knock down of lncRNA-CD244. Interestingly, adoptive transfer of lncRNA-CD244-depressed CD8(+) T cells to Mycobacterium tuberculosis (MTB)-infected mice reduced MTB infection and TB pathology compared with lncRNA-CD244-expressed controls. Thus, this work uncovers previously unidentified mechanisms in which T cell-inhibitory signaling and lncRNAs regulate T-cell responses and host defense against TB infection. Interferon-gamma - biosynthesis Polycomb Repressive Complex 2 - metabolism Promoter Regions, Genetic - genetics Protein Binding - drug effects Interferon-gamma - genetics CD8-Positive T-Lymphocytes - immunology Tumor Necrosis Factor-alpha - genetics RNA, Long Noncoding - genetics Tuberculosis - immunology Chromatin - metabolism Intracellular Signaling Peptides and Proteins - metabolism Apoptosis - genetics CD8-Positive T-Lymphocytes - cytology Up-Regulation - drug effects Tumor Necrosis Factor-alpha - biosynthesis Apoptosis - drug effects Signal Transduction - drug effects Immunity - drug effects Antibodies, Monoclonal - pharmacology Signal Transduction - genetics Transcription Factors - metabolism Immunity - genetics CD8-Positive T-Lymphocytes - drug effects Epigenesis, Genetic - drug effects Bacteria Chromatin Tuberculosis Correlation analysis Molecules Rodents T cell receptors Crystal Y. Chen oth Zheng W. Chen oth Xiaodan Xie oth Yang Wang oth Gucheng Zeng oth Huiling Zhong oth Ling Shen oth Hui Zhang oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 112(2015), 29, Seite E3883-E3892 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:112 year:2015 number:29 pages:E3883-E3892 http://dx.doi.org/10.1073/pnas.1501662112 Volltext http://www.pnas.org/content/112/29/E3883.abstract http://www.ncbi.nlm.nih.gov/pubmed/26150504 http://search.proquest.com/docview/1699087846 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-MAT SSG-OPC-FOR GBV_ILN_40 GBV_ILN_59 AR 112 2015 29 E3883-E3892 |
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10.1073/pnas.1501662112 doi PQ20160211 (DE-627)OLC1970275596 (DE-599)GBVOLC1970275596 (PRQ)c2289-7706fd17485ef0c4e0de2391ee1973f6d620c3e417d5f6449770c6a2a1727e1a3 (KEY)0583363920150000112002903883longnoncodingrnaderivedfromcd244signalingepigeneti DE-627 ger DE-627 rakwb eng 500 DNB 570 AVZ LING fid BIODIV fid Dan Huang verfasserin aut Long noncoding RNA derived from CD244 signaling epigenetically controls CD8+ T-cell immune responses in tuberculosis infection 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Molecular mechanisms for T-cell immune responses modulated by T cell-inhibitory molecules during tuberculosis (TB) infection remain unclear. Here, we show that active human TB infection up-regulates CD244 and CD244 signaling-associated molecules in CD8(+) T cells and that blockade of CD244 signaling enhances production of IFN-γ and TNF-α. CD244 expression/signaling in TB correlates with high levels of a long noncoding RNA (lncRNA)-BC050410 [named as lncRNA-AS-GSTT1(1-72) or lncRNA-CD244] in the CD244(+)CD8(+) T-cell subpopulation. CD244 signaling drives lncRNA-CD244 expression via sustaining a permissive chromatin state in the lncRNA-CD244 locus. By recruiting polycomb protein enhancer of zeste homolog 2 (EZH2) to infg/tnfa promoters, lncRNA-CD244 mediates H3K27 trimethylation at infg/tnfa loci toward repressive chromatin states and inhibits IFN-γ/TNF-α expression in CD8(+) T cells. Such inhibition can be reversed by knock down of lncRNA-CD244. Interestingly, adoptive transfer of lncRNA-CD244-depressed CD8(+) T cells to Mycobacterium tuberculosis (MTB)-infected mice reduced MTB infection and TB pathology compared with lncRNA-CD244-expressed controls. Thus, this work uncovers previously unidentified mechanisms in which T cell-inhibitory signaling and lncRNAs regulate T-cell responses and host defense against TB infection. Interferon-gamma - biosynthesis Polycomb Repressive Complex 2 - metabolism Promoter Regions, Genetic - genetics Protein Binding - drug effects Interferon-gamma - genetics CD8-Positive T-Lymphocytes - immunology Tumor Necrosis Factor-alpha - genetics RNA, Long Noncoding - genetics Tuberculosis - immunology Chromatin - metabolism Intracellular Signaling Peptides and Proteins - metabolism Apoptosis - genetics CD8-Positive T-Lymphocytes - cytology Up-Regulation - drug effects Tumor Necrosis Factor-alpha - biosynthesis Apoptosis - drug effects Signal Transduction - drug effects Immunity - drug effects Antibodies, Monoclonal - pharmacology Signal Transduction - genetics Transcription Factors - metabolism Immunity - genetics CD8-Positive T-Lymphocytes - drug effects Epigenesis, Genetic - drug effects Bacteria Chromatin Tuberculosis Correlation analysis Molecules Rodents T cell receptors Crystal Y. Chen oth Zheng W. Chen oth Xiaodan Xie oth Yang Wang oth Gucheng Zeng oth Huiling Zhong oth Ling Shen oth Hui Zhang oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 112(2015), 29, Seite E3883-E3892 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:112 year:2015 number:29 pages:E3883-E3892 http://dx.doi.org/10.1073/pnas.1501662112 Volltext http://www.pnas.org/content/112/29/E3883.abstract http://www.ncbi.nlm.nih.gov/pubmed/26150504 http://search.proquest.com/docview/1699087846 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-MAT SSG-OPC-FOR GBV_ILN_40 GBV_ILN_59 AR 112 2015 29 E3883-E3892 |
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Dan Huang |
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500 DNB 570 AVZ LING fid BIODIV fid Long noncoding RNA derived from CD244 signaling epigenetically controls CD8+ T-cell immune responses in tuberculosis infection Interferon-gamma - biosynthesis Polycomb Repressive Complex 2 - metabolism Promoter Regions, Genetic - genetics Protein Binding - drug effects Interferon-gamma - genetics CD8-Positive T-Lymphocytes - immunology Tumor Necrosis Factor-alpha - genetics RNA, Long Noncoding - genetics Tuberculosis - immunology Chromatin - metabolism Intracellular Signaling Peptides and Proteins - metabolism Apoptosis - genetics CD8-Positive T-Lymphocytes - cytology Up-Regulation - drug effects Tumor Necrosis Factor-alpha - biosynthesis Apoptosis - drug effects Signal Transduction - drug effects Immunity - drug effects Antibodies, Monoclonal - pharmacology Signal Transduction - genetics Transcription Factors - metabolism Immunity - genetics CD8-Positive T-Lymphocytes - drug effects Epigenesis, Genetic - drug effects Bacteria Chromatin Tuberculosis Correlation analysis Molecules Rodents T cell receptors |
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ddc 500 ddc 570 fid LING fid BIODIV misc Interferon-gamma - biosynthesis misc Polycomb Repressive Complex 2 - metabolism misc Promoter Regions, Genetic - genetics misc Protein Binding - drug effects misc Interferon-gamma - genetics misc CD8-Positive T-Lymphocytes - immunology misc Tumor Necrosis Factor-alpha - genetics misc RNA, Long Noncoding - genetics misc Tuberculosis - immunology misc Chromatin - metabolism misc Intracellular Signaling Peptides and Proteins - metabolism misc Apoptosis - genetics misc CD8-Positive T-Lymphocytes - cytology misc Up-Regulation - drug effects misc Tumor Necrosis Factor-alpha - biosynthesis misc Apoptosis - drug effects misc Signal Transduction - drug effects misc Immunity - drug effects misc Antibodies, Monoclonal - pharmacology misc Signal Transduction - genetics misc Transcription Factors - metabolism misc Immunity - genetics misc CD8-Positive T-Lymphocytes - drug effects misc Epigenesis, Genetic - drug effects misc Bacteria misc Chromatin misc Tuberculosis misc Correlation analysis misc Molecules misc Rodents misc T cell receptors |
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ddc 500 ddc 570 fid LING fid BIODIV misc Interferon-gamma - biosynthesis misc Polycomb Repressive Complex 2 - metabolism misc Promoter Regions, Genetic - genetics misc Protein Binding - drug effects misc Interferon-gamma - genetics misc CD8-Positive T-Lymphocytes - immunology misc Tumor Necrosis Factor-alpha - genetics misc RNA, Long Noncoding - genetics misc Tuberculosis - immunology misc Chromatin - metabolism misc Intracellular Signaling Peptides and Proteins - metabolism misc Apoptosis - genetics misc CD8-Positive T-Lymphocytes - cytology misc Up-Regulation - drug effects misc Tumor Necrosis Factor-alpha - biosynthesis misc Apoptosis - drug effects misc Signal Transduction - drug effects misc Immunity - drug effects misc Antibodies, Monoclonal - pharmacology misc Signal Transduction - genetics misc Transcription Factors - metabolism misc Immunity - genetics misc CD8-Positive T-Lymphocytes - drug effects misc Epigenesis, Genetic - drug effects misc Bacteria misc Chromatin misc Tuberculosis misc Correlation analysis misc Molecules misc Rodents misc T cell receptors |
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Long noncoding RNA derived from CD244 signaling epigenetically controls CD8+ T-cell immune responses in tuberculosis infection |
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Dan Huang |
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long noncoding rna derived from cd244 signaling epigenetically controls cd8+ t-cell immune responses in tuberculosis infection |
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Long noncoding RNA derived from CD244 signaling epigenetically controls CD8+ T-cell immune responses in tuberculosis infection |
| abstract |
Molecular mechanisms for T-cell immune responses modulated by T cell-inhibitory molecules during tuberculosis (TB) infection remain unclear. Here, we show that active human TB infection up-regulates CD244 and CD244 signaling-associated molecules in CD8(+) T cells and that blockade of CD244 signaling enhances production of IFN-γ and TNF-α. CD244 expression/signaling in TB correlates with high levels of a long noncoding RNA (lncRNA)-BC050410 [named as lncRNA-AS-GSTT1(1-72) or lncRNA-CD244] in the CD244(+)CD8(+) T-cell subpopulation. CD244 signaling drives lncRNA-CD244 expression via sustaining a permissive chromatin state in the lncRNA-CD244 locus. By recruiting polycomb protein enhancer of zeste homolog 2 (EZH2) to infg/tnfa promoters, lncRNA-CD244 mediates H3K27 trimethylation at infg/tnfa loci toward repressive chromatin states and inhibits IFN-γ/TNF-α expression in CD8(+) T cells. Such inhibition can be reversed by knock down of lncRNA-CD244. Interestingly, adoptive transfer of lncRNA-CD244-depressed CD8(+) T cells to Mycobacterium tuberculosis (MTB)-infected mice reduced MTB infection and TB pathology compared with lncRNA-CD244-expressed controls. Thus, this work uncovers previously unidentified mechanisms in which T cell-inhibitory signaling and lncRNAs regulate T-cell responses and host defense against TB infection. |
| abstractGer |
Molecular mechanisms for T-cell immune responses modulated by T cell-inhibitory molecules during tuberculosis (TB) infection remain unclear. Here, we show that active human TB infection up-regulates CD244 and CD244 signaling-associated molecules in CD8(+) T cells and that blockade of CD244 signaling enhances production of IFN-γ and TNF-α. CD244 expression/signaling in TB correlates with high levels of a long noncoding RNA (lncRNA)-BC050410 [named as lncRNA-AS-GSTT1(1-72) or lncRNA-CD244] in the CD244(+)CD8(+) T-cell subpopulation. CD244 signaling drives lncRNA-CD244 expression via sustaining a permissive chromatin state in the lncRNA-CD244 locus. By recruiting polycomb protein enhancer of zeste homolog 2 (EZH2) to infg/tnfa promoters, lncRNA-CD244 mediates H3K27 trimethylation at infg/tnfa loci toward repressive chromatin states and inhibits IFN-γ/TNF-α expression in CD8(+) T cells. Such inhibition can be reversed by knock down of lncRNA-CD244. Interestingly, adoptive transfer of lncRNA-CD244-depressed CD8(+) T cells to Mycobacterium tuberculosis (MTB)-infected mice reduced MTB infection and TB pathology compared with lncRNA-CD244-expressed controls. Thus, this work uncovers previously unidentified mechanisms in which T cell-inhibitory signaling and lncRNAs regulate T-cell responses and host defense against TB infection. |
| abstract_unstemmed |
Molecular mechanisms for T-cell immune responses modulated by T cell-inhibitory molecules during tuberculosis (TB) infection remain unclear. Here, we show that active human TB infection up-regulates CD244 and CD244 signaling-associated molecules in CD8(+) T cells and that blockade of CD244 signaling enhances production of IFN-γ and TNF-α. CD244 expression/signaling in TB correlates with high levels of a long noncoding RNA (lncRNA)-BC050410 [named as lncRNA-AS-GSTT1(1-72) or lncRNA-CD244] in the CD244(+)CD8(+) T-cell subpopulation. CD244 signaling drives lncRNA-CD244 expression via sustaining a permissive chromatin state in the lncRNA-CD244 locus. By recruiting polycomb protein enhancer of zeste homolog 2 (EZH2) to infg/tnfa promoters, lncRNA-CD244 mediates H3K27 trimethylation at infg/tnfa loci toward repressive chromatin states and inhibits IFN-γ/TNF-α expression in CD8(+) T cells. Such inhibition can be reversed by knock down of lncRNA-CD244. Interestingly, adoptive transfer of lncRNA-CD244-depressed CD8(+) T cells to Mycobacterium tuberculosis (MTB)-infected mice reduced MTB infection and TB pathology compared with lncRNA-CD244-expressed controls. Thus, this work uncovers previously unidentified mechanisms in which T cell-inhibitory signaling and lncRNAs regulate T-cell responses and host defense against TB infection. |
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Long noncoding RNA derived from CD244 signaling epigenetically controls CD8+ T-cell immune responses in tuberculosis infection |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a2200265 4500</leader><controlfield tag="001">OLC1970275596</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230714175930.0</controlfield><controlfield tag="007">tu</controlfield><controlfield tag="008">160211s2015 xx ||||| 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1073/pnas.1501662112</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">PQ20160211</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)OLC1970275596</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)GBVOLC1970275596</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(PRQ)c2289-7706fd17485ef0c4e0de2391ee1973f6d620c3e417d5f6449770c6a2a1727e1a3</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(KEY)0583363920150000112002903883longnoncodingrnaderivedfromcd244signalingepigeneti</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">500</subfield><subfield code="q">DNB</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">570</subfield><subfield code="q">AVZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">LING</subfield><subfield code="2">fid</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">BIODIV</subfield><subfield code="2">fid</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Dan Huang</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Long noncoding RNA derived from CD244 signaling epigenetically controls CD8+ T-cell immune responses in tuberculosis infection</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2015</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">ohne Hilfsmittel zu benutzen</subfield><subfield code="b">n</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Band</subfield><subfield code="b">nc</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Molecular mechanisms for T-cell immune responses modulated by T cell-inhibitory molecules during tuberculosis (TB) infection remain unclear. Here, we show that active human TB infection up-regulates CD244 and CD244 signaling-associated molecules in CD8(+) T cells and that blockade of CD244 signaling enhances production of IFN-γ and TNF-α. CD244 expression/signaling in TB correlates with high levels of a long noncoding RNA (lncRNA)-BC050410 [named as lncRNA-AS-GSTT1(1-72) or lncRNA-CD244] in the CD244(+)CD8(+) T-cell subpopulation. CD244 signaling drives lncRNA-CD244 expression via sustaining a permissive chromatin state in the lncRNA-CD244 locus. By recruiting polycomb protein enhancer of zeste homolog 2 (EZH2) to infg/tnfa promoters, lncRNA-CD244 mediates H3K27 trimethylation at infg/tnfa loci toward repressive chromatin states and inhibits IFN-γ/TNF-α expression in CD8(+) T cells. Such inhibition can be reversed by knock down of lncRNA-CD244. Interestingly, adoptive transfer of lncRNA-CD244-depressed CD8(+) T cells to Mycobacterium tuberculosis (MTB)-infected mice reduced MTB infection and TB pathology compared with lncRNA-CD244-expressed controls. Thus, this work uncovers previously unidentified mechanisms in which T cell-inhibitory signaling and lncRNAs regulate T-cell responses and host defense against TB infection.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Interferon-gamma - biosynthesis</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Polycomb Repressive Complex 2 - metabolism</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Promoter Regions, Genetic - genetics</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Protein Binding - drug effects</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Interferon-gamma - genetics</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">CD8-Positive T-Lymphocytes - immunology</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Tumor Necrosis Factor-alpha - genetics</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">RNA, Long Noncoding - genetics</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Tuberculosis - immunology</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Chromatin - metabolism</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Intracellular Signaling Peptides and Proteins - metabolism</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Apoptosis - genetics</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">CD8-Positive T-Lymphocytes - cytology</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Up-Regulation - drug effects</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Tumor Necrosis Factor-alpha - biosynthesis</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Apoptosis - drug effects</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Signal Transduction - drug effects</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Immunity - drug effects</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Antibodies, Monoclonal - pharmacology</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Signal Transduction - genetics</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Transcription Factors - metabolism</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Immunity - genetics</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">CD8-Positive T-Lymphocytes - drug effects</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Epigenesis, Genetic - drug effects</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Bacteria</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Chromatin</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Tuberculosis</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Correlation analysis</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Molecules</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Rodents</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">T cell receptors</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Crystal Y. Chen</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Zheng W. Chen</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Xiaodan Xie</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Yang Wang</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Gucheng Zeng</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Huiling Zhong</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Ling Shen</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Hui Zhang</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Proceedings of the National Academy of Sciences of the United States of America</subfield><subfield code="d">Washington, DC : NAS, 1877</subfield><subfield code="g">112(2015), 29, Seite E3883-E3892</subfield><subfield code="w">(DE-627)129505269</subfield><subfield code="w">(DE-600)209104-5</subfield><subfield code="w">(DE-576)014909189</subfield><subfield code="x">0027-8424</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:112</subfield><subfield code="g">year:2015</subfield><subfield code="g">number:29</subfield><subfield code="g">pages:E3883-E3892</subfield></datafield><datafield tag="856" ind1="4" ind2="1"><subfield code="u">http://dx.doi.org/10.1073/pnas.1501662112</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">http://www.pnas.org/content/112/29/E3883.abstract</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">http://www.ncbi.nlm.nih.gov/pubmed/26150504</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">http://search.proquest.com/docview/1699087846</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">FID-LING</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">FID-BIODIV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHY</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-CHE</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-MAT</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-FOR</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="912" ind1=" " ind2=" "><subfield code="a">SSG-OPC-MAT</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OPC-FOR</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_40</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_59</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">112</subfield><subfield code="j">2015</subfield><subfield code="e">29</subfield><subfield code="h">E3883-E3892</subfield></datafield></record></collection>
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