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Programmed cell death protein-1 (PD1) expresses on the cell surface of the activated lymphocytes and at least a subset of Foxp3+ regulatory T cells. The binding of PD1 to its ligands including PD-L1 and PD-L2 leads to deliver an inhibitory signal to the activated cells. Although PD1/PD-L signal deficiency can lead to failure in the self-tolerance and development of autoimmunity disorders, PD1 blockade with monoclonal antibodies is considered an effective strategy in cancer immunotherapy. Determining effective environmental factors such as stress conditions on the expression of PD1 and PD-L1 genes can provide an immunotherapeutic strategy to control PD1 signaling in the patients Mammalian target of rapamycin signaling is a stress-responsive pathway in the cells that can be blocked by rapamycin. In this study, the effects of rapamycin on the expression of immunoregulatory genes were investigated in the stress condition.

research in pharmaceutical sciences

Rapamycin attenuates gene expression of programmed cell death protein-ligand 1 and Foxp3 in the brain; a novel mechanism proposed for immunotherapy in the brain