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The mechanism of rapamycin in promoting asthmatic regulatory T cell differentiation and function / 浙江大学学报·医学版
Journal of Zhejiang University. Medical sciences ; (6): 621-626, 2021.
Artigo em Inglês | WPRIM | ID: wpr-922250
ABSTRACT
To investigate the mechanism of rapamycin in promoting asthmatic regulatory T cell differentiation . Asthma model was prepared by sensitization and challenge of ovalbumin in mice. Spleen CD4CD25 T cells were sorted from the asthmatic mice and normal mice by ultrahigh speed flow cytometer, and divided into three groups. Transforming growth factor-β and interleukin-2, or combined with rapamycin (final concentration of 500 nmol/L) were given in the model group or the rapamycin group. The levels of Treg cells and CD4CD25 T cells were detected by flow cytometry. The phosphorylation level of downstream proteins of S6 and Akt in the mTORC1/2 signaling pathway were examined by Western blotting. Compared with the model group, the differentiation level of Treg cells in the rapamycin group was significantly increased, the proliferation level of CD4CD25 T cells was decreased, and the phosphorylations of the mTORC1/2 substrates, S6 protein and Akt were decreased (all <0.05). Rapamycin can promote the differentiation and function of Treg cells via inhibition of the mTORC1/2 signaling pathway.
Assuntos

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Fosforilação / Asma / Transdução de Sinais / Diferenciação Celular / Linfócitos T Reguladores / Sirolimo Tipo de estudo: Estudo prognóstico Limite: Animais Idioma: Inglês Revista: Journal of Zhejiang University. Medical sciences Ano de publicação: 2021 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Fosforilação / Asma / Transdução de Sinais / Diferenciação Celular / Linfócitos T Reguladores / Sirolimo Tipo de estudo: Estudo prognóstico Limite: Animais Idioma: Inglês Revista: Journal of Zhejiang University. Medical sciences Ano de publicação: 2021 Tipo de documento: Artigo