JunB is essential for IL-23-dependent pathogenicity of Th17 cells
T helper 17 (Th17) cells can be pathogenic, but what controls this phenotype is unclear. Here the authors show that the transcription factor JunB promotes proinflammatory Th17 function by regulating the transcription of multiple Th17-related genes.
Guardado en:
Autores principales: | Zafrul Hasan, Shin-ichi Koizumi, Daiki Sasaki, Hayato Yamada, Nana Arakaki, Yoshitaka Fujihara, Shiho Okitsu, Hiroki Shirahata, Hiroki Ishikawa |
---|---|
Formato: | article |
Lenguaje: | EN |
Publicado: |
Nature Portfolio
2017
|
Materias: | |
Acceso en línea: | https://doaj.org/article/68b10b31b4c2404e89ca812ba7589cc1 |
Etiquetas: |
Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
|
Ejemplares similares
-
JunB regulates homeostasis and suppressive functions of effector regulatory T cells
por: Shin-ichi Koizumi, et al.
Publicado: (2018) -
JunB promotes Th17 cell identity and restrains alternative CD4+ T-cell programs during inflammation
por: Tiffany M. Carr, et al.
Publicado: (2017) -
JunB defines functional and structural integrity of the epidermo-pilosebaceous unit in the skin
por: Karmveer Singh, et al.
Publicado: (2018) -
Epidermal chloroplasts are defense-related motile organelles equipped with plant immune components
por: Hiroki Irieda, et al.
Publicado: (2021) -
Development of LORL evaluation method and its application to a loop-type sodium-cooled fast reactor
por: Yuya IMAIZUMI, et al.
Publicado: (2018)