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.
Subject(s)
Animals , Mice , Asthma , Cell Differentiation , Phosphorylation , Signal Transduction , Sirolimus/pharmacology , T-Lymphocytes, RegulatoryABSTRACT
Polycystic ovary syndrome (PCOS) is an endocrine disorder with a variety of etiopathogensis and clinic manifestations. Hitherto its pathogenesy is still uncleared. However, there have been increasing supports for the contribution of the hyperinsulinism and hyperandrogenaemia in the pathological process of the PCOS. Recent years, some literatures reported that hyperleptinaemia is also an important factor. This review seeks to bring together the pothogenesy of the PCOS with these factors.