Balanced Bcl-3 expression in murine CD4+ T cells is required for generation of encephalitogenic Th17 cells
© 2017 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim..
The function of NF-κB family members is controlled by multiple mechanisms including the transcriptional regulator Bcl-3, an atypical member of the IκB family. By using a murine model of conditional Bcl-3 overexpression specifically in T cells, we observed impairment in the development of Th2, Th1, and Th17 cells. High expression of Bcl-3 promoted CD4+ T-cell survival, but at the same time suppressed proliferation in response to TCR stimulation, resulting in reduced CD4+ T-cell expansion. As a consequence, T-cell-specific overexpression of Bcl-3 led to reduced inflammation in the small intestine of mice applied with anti-CD3 in a model of gut inflammation. Moreover, impaired Th17-cell development resulted in the resistance of Bcl-3 overexpressing mice to EAE, a mouse model of multiple sclerosis. Thus, we concluded that fine-tuning expression of Bcl-3 is needed for proper CD4+ T-cell development and is required to sustain Th17-cell mediated pathology.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2017 |
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| Erschienen: |
2017 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:47 |
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| Enthalten in: |
European journal of immunology - 47(2017), 8 vom: 09. Aug., Seite 1335-1341 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Mufazalov, Ilgiz A [VerfasserIn] |
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| Links: |
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| Themen: |
Anti-CD3 treatment |
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| Anmerkungen: |
Date Completed 16.10.2017 Date Revised 10.12.2019 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1002/eji.201746933 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM272780219 |
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| 520 | |a © 2017 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim. | ||
| 520 | |a The function of NF-κB family members is controlled by multiple mechanisms including the transcriptional regulator Bcl-3, an atypical member of the IκB family. By using a murine model of conditional Bcl-3 overexpression specifically in T cells, we observed impairment in the development of Th2, Th1, and Th17 cells. High expression of Bcl-3 promoted CD4+ T-cell survival, but at the same time suppressed proliferation in response to TCR stimulation, resulting in reduced CD4+ T-cell expansion. As a consequence, T-cell-specific overexpression of Bcl-3 led to reduced inflammation in the small intestine of mice applied with anti-CD3 in a model of gut inflammation. Moreover, impaired Th17-cell development resulted in the resistance of Bcl-3 overexpressing mice to EAE, a mouse model of multiple sclerosis. Thus, we concluded that fine-tuning expression of Bcl-3 is needed for proper CD4+ T-cell development and is required to sustain Th17-cell mediated pathology | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Bcl-3 | |
| 650 | 4 | |a EAE | |
| 650 | 4 | |a MOG | |
| 650 | 4 | |a NF-κB | |
| 650 | 4 | |a Th17 cells | |
| 650 | 4 | |a T cells | |
| 650 | 4 | |a anti-CD3 treatment | |
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| 700 | 1 | |a Kuschmann, Janina |e verfasserin |4 aut | |
| 700 | 1 | |a Andruszewski, David |e verfasserin |4 aut | |
| 700 | 1 | |a Masri, Joumana |e verfasserin |4 aut | |
| 700 | 1 | |a Gabriel, Laureen A |e verfasserin |4 aut | |
| 700 | 1 | |a Adams, Petra |e verfasserin |4 aut | |
| 700 | 1 | |a Reissig, Sonja |e verfasserin |4 aut | |
| 700 | 1 | |a Hövelmeyer, Nadine |e verfasserin |4 aut | |
| 700 | 1 | |a Waisman, Ari |e verfasserin |4 aut | |
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