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Balanced Bcl-3 expression in murine CD4+ T cells is required for generation of encephalitogenic Th17 cells.
Mufazalov, Ilgiz A; Kuschmann, Janina; Andruszewski, David; Masri, Joumana; Gabriel, Laureen A; Adams, Petra; Reissig, Sonja; Hövelmeyer, Nadine; Waisman, Ari.
Afiliación
  • Mufazalov IA; Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
  • Kuschmann J; Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
  • Andruszewski D; Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
  • Masri J; Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
  • Gabriel LA; Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
  • Adams P; Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
  • Reissig S; Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
  • Hövelmeyer N; Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
  • Waisman A; Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
Eur J Immunol ; 47(8): 1335-1341, 2017 08.
Article en En | MEDLINE | ID: mdl-28598502
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.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Factores de Transcripción / Linfocitos T CD4-Positivos / Proteínas Proto-Oncogénicas / Encefalomielitis Autoinmune Experimental / Células Th17 Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Eur J Immunol Año: 2017 Tipo del documento: Article País de afiliación: Alemania

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Factores de Transcripción / Linfocitos T CD4-Positivos / Proteínas Proto-Oncogénicas / Encefalomielitis Autoinmune Experimental / Células Th17 Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Eur J Immunol Año: 2017 Tipo del documento: Article País de afiliación: Alemania
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