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.