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Cancer Immunol Immunother. 2015 Nov;64(11):1383-92. doi: 10.1007/s00262-015-1740-2. Epub 2015 Jul 17.

Surgical trauma induces postoperative T-cell dysfunction in lung cancer patients through the programmed death-1 pathway.

Author information

1
Department of Anesthesiology, Fudan University Shanghai Cancer Center, No. 270, Dong an Road, Shanghai, 200032, People's Republic of China.
2
Cancer Institute, Fudan University Shanghai Cancer Center, No. 270, Dong an Road, Shanghai, 200032, People's Republic of China.
3
Department of Anesthesiology, Fudan University Shanghai Cancer Center, No. 270, Dong an Road, Shanghai, 200032, People's Republic of China. changhongmiaosh@163.com.

Abstract

The programmed death-1 (PD-1) and programmed death ligand-1 (PD-L1) pathway have been shown to be involved in tumor-induced and sepsis-induced immunosuppression. However, whether this pathway is involved in the surgery-induced dysfunction of T lymphocytes is not known. Here, we analyzed expression of PD-1 and PD-L1 on human peripheral mononuclear cells during the perioperative period. We found that surgery increased PD-1/PD-L1 expression on immune cells, which was correlated with the severity of surgical trauma. The count of T lymphocytes and natural killer cells reduced after surgery, probably due to the increased activity of caspase-3. Caspase-3 level was positively correlated with PD-1 expression. Profile of perioperative cytokines and hormones in plasma showed a significantly increased level of interferon-α, as well as various inflammatory cytokines and stress hormones. In ex vivo experiments, administration of anti-PD-1 antibody significantly ameliorated T-cell proliferation and partially reversed the T-cell apoptosis induced by surgical trauma. We provide evidences that surgical trauma can induce immunosuppression through the PD-1/PD-L1 pathway. This pathway could be a target for preventing postoperative cellular immunosuppression.

KEYWORDS:

Immunosuppression; Lung cancer; PD-1/PD-L1; Surgery

PMID:
26183035
DOI:
10.1007/s00262-015-1740-2
[Indexed for MEDLINE]

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