RelB regulates Th17 differentiation in a cell-intrinsic manner.
Immunobiology
; 223(2): 191-199, 2018 02.
Article
en En
| MEDLINE
| ID: mdl-29050819
ABSTRACT
The role of the alternative NF-κB pathway is mainly attributed to the lymphoid organ formation and blood cancer. However, its involvement in lymphocyte differentiation is not clearly defined. Recently, we have shown that uncontrolled activation of alternative NF-κB in mice lacking the NF-κB inhibitory protein p100 (p100-/- mice) hinders plasmablast proliferation and diminishes T cell independent responses. Here we show that hyperactivation of this pathway leads to a cell-intrinsic T cell defects. p100-deficient T helper cells displayed both an activation and a proliferation defect in vitro. In addition, memory T cell formation was impaired in vivo. Moreover, p100-/- T cells failed to polarize into T helper 17 cells. This phenotype was dependent on increased RelB activation and suboptimal RORγt expression. Thus, our results demonstrate that RelB acts as a negative regulator of T cell activation and Th17 development. Targeting this pathway therefore could be beneficial in Th17-mediated pathologies.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Células Plasmáticas
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Enfermedades Autoinmunes
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Linfocitos B
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Subgrupos de Linfocitos T
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Factor de Transcripción ReIB
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Células Th17
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Inflamación
Límite:
Animals
Idioma:
En
Revista:
Immunobiology
Año:
2018
Tipo del documento:
Article