The mechanism of rapamycin in promoting asthmatic regulatory T cell differentiation and function.
10.3724/zdxbyxb-2021-0173
- Author:
Hualiang JIN
1
;
Yan ZHOU
1
;
Limin WANG
1
Author Information
1. Department of Respiratory Medicine, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou 310006, China.
- Publication Type:Journal Article
- Keywords:
Asthma;
Differentiation;
Mammalian target of rapamycin;
Proliferation;
experiment;
Rapamycin;
Regulatory T cell
- MeSH:
Animals;
Asthma;
Cell Differentiation;
Mice;
Phosphorylation;
Signal Transduction;
Sirolimus/pharmacology*;
T-Lymphocytes, Regulatory
- From:
Journal of Zhejiang University. Medical sciences
2021;50(5):621-626
- CountryChina
- Language:English
-
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.
