Canonical NF-[kappa]B signaling is uniquely required for the long-term persistence of functional mature b cells
Although canonical NF-[kappa]B signaling is crucial to generate a normal mature B-cell compartment, its role in the persistence of resting mature B cells is controversial. To resolve this conflict, we ablated NF-[kappa]B essential modulator (NEMO) and IkB kinase 2 (IKK2), two essential mediators of...
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Gespeichert in:
| Autor*in: |
Derudder, Emmanuel [verfasserIn] |
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| Format: |
Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2016 |
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| Rechteinformationen: |
Nutzungsrecht: © COPYRIGHT 2016 National Academy of Sciences |
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| Schlagwörter: |
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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, 113(2016), 18, Seite 5065 |
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| Übergeordnetes Werk: |
volume:113 ; year:2016 ; number:18 ; pages:5065 |
| Links: |
|---|
| DOI / URN: |
10.1073/pnas.1604529113 |
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OLC1978649479 |
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| 520 | |a Although canonical NF-[kappa]B signaling is crucial to generate a normal mature B-cell compartment, its role in the persistence of resting mature B cells is controversial. To resolve this conflict, we ablated NF-[kappa]B essential modulator (NEMO) and IkB kinase 2 (IKK2), two essential mediators of the canonical pathway, either early on in B-cell development or specifically in mature B cells. Early ablation severely inhibited the generation of all mature B-cell subsets, but follicular B-cell numbers could be largely rescued by ectopic expression of B-cell lymphoma 2 (Bcl2), despite a persisting block at the transitional stage. Marginal zone (MZ) B and B1 cells were not rescued, indicating a possible role of canonical NF-[kappa]B signals beyond the control of cell survival in these subsets. When canonical NF-[kappa]B signaling was ablated specifically in mature B cells, the differentiation and/or persistence of MZ B cells was still abrogated, but follicular B-cell numbers were only mildly affected. However, the mutant cells exhibited increased turnover as well as functional deficiencies upon activation, suggesting that canonical NF-[kappa]B signals contribute to their long-term persistence and functional fitness. | ||
| 540 | |a Nutzungsrecht: © COPYRIGHT 2016 National Academy of Sciences | ||
| 650 | 4 | |a Research | |
| 650 | 4 | |a Cellular signal transduction | |
| 650 | 4 | |a B cells | |
| 650 | 4 | |a Immunological research | |
| 650 | 4 | |a Transcription factors | |
| 650 | 4 | |a Physiological aspects | |
| 650 | 4 | |a Gene expression | |
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| 700 | 1 | |a Herzog, Sebastian |4 oth | |
| 700 | 1 | |a Labi, Verena |4 oth | |
| 700 | 1 | |a Yasuda, Tomoharu |4 oth | |
| 700 | 1 | |a Kochert, Karl |4 oth | |
| 700 | 1 | |a Janz, Martin |4 oth | |
| 700 | 1 | |a Villunger, Andreas |4 oth | |
| 700 | 1 | |a Schmidt-Supprian, Marc |4 oth | |
| 700 | 1 | |a Rajewsky, Klaus |4 oth | |
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10.1073/pnas.1604529113 doi PQ20160719 (DE-627)OLC1978649479 (DE-599)GBVOLC1978649479 (PRQ)g513-d670415a821b8af346f18bfe4ff5e7b3d797d238c37ac1d5340cc2d42958b240 (KEY)0583363920160000113001805065canonicalnfkappabsignalingisuniquelyrequiredforthe DE-627 ger DE-627 rakwb eng 500 DNB 570 AVZ LING fid BIODIV fid Derudder, Emmanuel verfasserin aut Canonical NF-[kappa]B signaling is uniquely required for the long-term persistence of functional mature b cells 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Although canonical NF-[kappa]B signaling is crucial to generate a normal mature B-cell compartment, its role in the persistence of resting mature B cells is controversial. To resolve this conflict, we ablated NF-[kappa]B essential modulator (NEMO) and IkB kinase 2 (IKK2), two essential mediators of the canonical pathway, either early on in B-cell development or specifically in mature B cells. Early ablation severely inhibited the generation of all mature B-cell subsets, but follicular B-cell numbers could be largely rescued by ectopic expression of B-cell lymphoma 2 (Bcl2), despite a persisting block at the transitional stage. Marginal zone (MZ) B and B1 cells were not rescued, indicating a possible role of canonical NF-[kappa]B signals beyond the control of cell survival in these subsets. When canonical NF-[kappa]B signaling was ablated specifically in mature B cells, the differentiation and/or persistence of MZ B cells was still abrogated, but follicular B-cell numbers were only mildly affected. However, the mutant cells exhibited increased turnover as well as functional deficiencies upon activation, suggesting that canonical NF-[kappa]B signals contribute to their long-term persistence and functional fitness. Nutzungsrecht: © COPYRIGHT 2016 National Academy of Sciences Research Cellular signal transduction B cells Immunological research Transcription factors Physiological aspects Gene expression Cells Signal transduction Herzog, Sebastian oth Labi, Verena oth Yasuda, Tomoharu oth Kochert, Karl oth Janz, Martin oth Villunger, Andreas oth Schmidt-Supprian, Marc oth Rajewsky, Klaus oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 113(2016), 18, Seite 5065 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:113 year:2016 number:18 pages:5065 http://dx.doi.org/10.1073/pnas.1604529113 Volltext http://search.proquest.com/docview/1801623973 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 113 2016 18 5065 |
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10.1073/pnas.1604529113 doi PQ20160719 (DE-627)OLC1978649479 (DE-599)GBVOLC1978649479 (PRQ)g513-d670415a821b8af346f18bfe4ff5e7b3d797d238c37ac1d5340cc2d42958b240 (KEY)0583363920160000113001805065canonicalnfkappabsignalingisuniquelyrequiredforthe DE-627 ger DE-627 rakwb eng 500 DNB 570 AVZ LING fid BIODIV fid Derudder, Emmanuel verfasserin aut Canonical NF-[kappa]B signaling is uniquely required for the long-term persistence of functional mature b cells 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Although canonical NF-[kappa]B signaling is crucial to generate a normal mature B-cell compartment, its role in the persistence of resting mature B cells is controversial. To resolve this conflict, we ablated NF-[kappa]B essential modulator (NEMO) and IkB kinase 2 (IKK2), two essential mediators of the canonical pathway, either early on in B-cell development or specifically in mature B cells. Early ablation severely inhibited the generation of all mature B-cell subsets, but follicular B-cell numbers could be largely rescued by ectopic expression of B-cell lymphoma 2 (Bcl2), despite a persisting block at the transitional stage. Marginal zone (MZ) B and B1 cells were not rescued, indicating a possible role of canonical NF-[kappa]B signals beyond the control of cell survival in these subsets. When canonical NF-[kappa]B signaling was ablated specifically in mature B cells, the differentiation and/or persistence of MZ B cells was still abrogated, but follicular B-cell numbers were only mildly affected. However, the mutant cells exhibited increased turnover as well as functional deficiencies upon activation, suggesting that canonical NF-[kappa]B signals contribute to their long-term persistence and functional fitness. Nutzungsrecht: © COPYRIGHT 2016 National Academy of Sciences Research Cellular signal transduction B cells Immunological research Transcription factors Physiological aspects Gene expression Cells Signal transduction Herzog, Sebastian oth Labi, Verena oth Yasuda, Tomoharu oth Kochert, Karl oth Janz, Martin oth Villunger, Andreas oth Schmidt-Supprian, Marc oth Rajewsky, Klaus oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 113(2016), 18, Seite 5065 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:113 year:2016 number:18 pages:5065 http://dx.doi.org/10.1073/pnas.1604529113 Volltext http://search.proquest.com/docview/1801623973 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 113 2016 18 5065 |
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10.1073/pnas.1604529113 doi PQ20160719 (DE-627)OLC1978649479 (DE-599)GBVOLC1978649479 (PRQ)g513-d670415a821b8af346f18bfe4ff5e7b3d797d238c37ac1d5340cc2d42958b240 (KEY)0583363920160000113001805065canonicalnfkappabsignalingisuniquelyrequiredforthe DE-627 ger DE-627 rakwb eng 500 DNB 570 AVZ LING fid BIODIV fid Derudder, Emmanuel verfasserin aut Canonical NF-[kappa]B signaling is uniquely required for the long-term persistence of functional mature b cells 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Although canonical NF-[kappa]B signaling is crucial to generate a normal mature B-cell compartment, its role in the persistence of resting mature B cells is controversial. To resolve this conflict, we ablated NF-[kappa]B essential modulator (NEMO) and IkB kinase 2 (IKK2), two essential mediators of the canonical pathway, either early on in B-cell development or specifically in mature B cells. Early ablation severely inhibited the generation of all mature B-cell subsets, but follicular B-cell numbers could be largely rescued by ectopic expression of B-cell lymphoma 2 (Bcl2), despite a persisting block at the transitional stage. Marginal zone (MZ) B and B1 cells were not rescued, indicating a possible role of canonical NF-[kappa]B signals beyond the control of cell survival in these subsets. When canonical NF-[kappa]B signaling was ablated specifically in mature B cells, the differentiation and/or persistence of MZ B cells was still abrogated, but follicular B-cell numbers were only mildly affected. However, the mutant cells exhibited increased turnover as well as functional deficiencies upon activation, suggesting that canonical NF-[kappa]B signals contribute to their long-term persistence and functional fitness. Nutzungsrecht: © COPYRIGHT 2016 National Academy of Sciences Research Cellular signal transduction B cells Immunological research Transcription factors Physiological aspects Gene expression Cells Signal transduction Herzog, Sebastian oth Labi, Verena oth Yasuda, Tomoharu oth Kochert, Karl oth Janz, Martin oth Villunger, Andreas oth Schmidt-Supprian, Marc oth Rajewsky, Klaus oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 113(2016), 18, Seite 5065 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:113 year:2016 number:18 pages:5065 http://dx.doi.org/10.1073/pnas.1604529113 Volltext http://search.proquest.com/docview/1801623973 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 113 2016 18 5065 |
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10.1073/pnas.1604529113 doi PQ20160719 (DE-627)OLC1978649479 (DE-599)GBVOLC1978649479 (PRQ)g513-d670415a821b8af346f18bfe4ff5e7b3d797d238c37ac1d5340cc2d42958b240 (KEY)0583363920160000113001805065canonicalnfkappabsignalingisuniquelyrequiredforthe DE-627 ger DE-627 rakwb eng 500 DNB 570 AVZ LING fid BIODIV fid Derudder, Emmanuel verfasserin aut Canonical NF-[kappa]B signaling is uniquely required for the long-term persistence of functional mature b cells 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Although canonical NF-[kappa]B signaling is crucial to generate a normal mature B-cell compartment, its role in the persistence of resting mature B cells is controversial. To resolve this conflict, we ablated NF-[kappa]B essential modulator (NEMO) and IkB kinase 2 (IKK2), two essential mediators of the canonical pathway, either early on in B-cell development or specifically in mature B cells. Early ablation severely inhibited the generation of all mature B-cell subsets, but follicular B-cell numbers could be largely rescued by ectopic expression of B-cell lymphoma 2 (Bcl2), despite a persisting block at the transitional stage. Marginal zone (MZ) B and B1 cells were not rescued, indicating a possible role of canonical NF-[kappa]B signals beyond the control of cell survival in these subsets. When canonical NF-[kappa]B signaling was ablated specifically in mature B cells, the differentiation and/or persistence of MZ B cells was still abrogated, but follicular B-cell numbers were only mildly affected. However, the mutant cells exhibited increased turnover as well as functional deficiencies upon activation, suggesting that canonical NF-[kappa]B signals contribute to their long-term persistence and functional fitness. Nutzungsrecht: © COPYRIGHT 2016 National Academy of Sciences Research Cellular signal transduction B cells Immunological research Transcription factors Physiological aspects Gene expression Cells Signal transduction Herzog, Sebastian oth Labi, Verena oth Yasuda, Tomoharu oth Kochert, Karl oth Janz, Martin oth Villunger, Andreas oth Schmidt-Supprian, Marc oth Rajewsky, Klaus oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 113(2016), 18, Seite 5065 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:113 year:2016 number:18 pages:5065 http://dx.doi.org/10.1073/pnas.1604529113 Volltext http://search.proquest.com/docview/1801623973 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 113 2016 18 5065 |
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canonical nf-[kappa]b signaling is uniquely required for the long-term persistence of functional mature b cells |
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Canonical NF-[kappa]B signaling is uniquely required for the long-term persistence of functional mature b cells |
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Although canonical NF-[kappa]B signaling is crucial to generate a normal mature B-cell compartment, its role in the persistence of resting mature B cells is controversial. To resolve this conflict, we ablated NF-[kappa]B essential modulator (NEMO) and IkB kinase 2 (IKK2), two essential mediators of the canonical pathway, either early on in B-cell development or specifically in mature B cells. Early ablation severely inhibited the generation of all mature B-cell subsets, but follicular B-cell numbers could be largely rescued by ectopic expression of B-cell lymphoma 2 (Bcl2), despite a persisting block at the transitional stage. Marginal zone (MZ) B and B1 cells were not rescued, indicating a possible role of canonical NF-[kappa]B signals beyond the control of cell survival in these subsets. When canonical NF-[kappa]B signaling was ablated specifically in mature B cells, the differentiation and/or persistence of MZ B cells was still abrogated, but follicular B-cell numbers were only mildly affected. However, the mutant cells exhibited increased turnover as well as functional deficiencies upon activation, suggesting that canonical NF-[kappa]B signals contribute to their long-term persistence and functional fitness. |
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Although canonical NF-[kappa]B signaling is crucial to generate a normal mature B-cell compartment, its role in the persistence of resting mature B cells is controversial. To resolve this conflict, we ablated NF-[kappa]B essential modulator (NEMO) and IkB kinase 2 (IKK2), two essential mediators of the canonical pathway, either early on in B-cell development or specifically in mature B cells. Early ablation severely inhibited the generation of all mature B-cell subsets, but follicular B-cell numbers could be largely rescued by ectopic expression of B-cell lymphoma 2 (Bcl2), despite a persisting block at the transitional stage. Marginal zone (MZ) B and B1 cells were not rescued, indicating a possible role of canonical NF-[kappa]B signals beyond the control of cell survival in these subsets. When canonical NF-[kappa]B signaling was ablated specifically in mature B cells, the differentiation and/or persistence of MZ B cells was still abrogated, but follicular B-cell numbers were only mildly affected. However, the mutant cells exhibited increased turnover as well as functional deficiencies upon activation, suggesting that canonical NF-[kappa]B signals contribute to their long-term persistence and functional fitness. |
| abstract_unstemmed |
Although canonical NF-[kappa]B signaling is crucial to generate a normal mature B-cell compartment, its role in the persistence of resting mature B cells is controversial. To resolve this conflict, we ablated NF-[kappa]B essential modulator (NEMO) and IkB kinase 2 (IKK2), two essential mediators of the canonical pathway, either early on in B-cell development or specifically in mature B cells. Early ablation severely inhibited the generation of all mature B-cell subsets, but follicular B-cell numbers could be largely rescued by ectopic expression of B-cell lymphoma 2 (Bcl2), despite a persisting block at the transitional stage. Marginal zone (MZ) B and B1 cells were not rescued, indicating a possible role of canonical NF-[kappa]B signals beyond the control of cell survival in these subsets. When canonical NF-[kappa]B signaling was ablated specifically in mature B cells, the differentiation and/or persistence of MZ B cells was still abrogated, but follicular B-cell numbers were only mildly affected. However, the mutant cells exhibited increased turnover as well as functional deficiencies upon activation, suggesting that canonical NF-[kappa]B signals contribute to their long-term persistence and functional fitness. |
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Canonical NF-[kappa]B signaling is uniquely required for the long-term persistence of functional mature b cells |
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However, the mutant cells exhibited increased turnover as well as functional deficiencies upon activation, suggesting that canonical NF-[kappa]B signals contribute to their long-term persistence and functional fitness.</subfield></datafield><datafield tag="540" ind1=" " ind2=" "><subfield code="a">Nutzungsrecht: © COPYRIGHT 2016 National Academy of Sciences</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Research</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Cellular signal transduction</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">B cells</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Immunological research</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Transcription factors</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Physiological aspects</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Gene expression</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Cells</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Signal transduction</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Herzog, Sebastian</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Labi, Verena</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yasuda, Tomoharu</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kochert, Karl</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Janz, Martin</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Villunger, Andreas</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Schmidt-Supprian, Marc</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Rajewsky, Klaus</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">113(2016), 18, Seite 5065</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:113</subfield><subfield code="g">year:2016</subfield><subfield code="g">number:18</subfield><subfield code="g">pages:5065</subfield></datafield><datafield tag="856" ind1="4" ind2="1"><subfield code="u">http://dx.doi.org/10.1073/pnas.1604529113</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">http://search.proquest.com/docview/1801623973</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">113</subfield><subfield code="j">2016</subfield><subfield code="e">18</subfield><subfield code="h">5065</subfield></datafield></record></collection>
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