title: Increased soluble and membrane-bound PD-L1 contributes to immune regulation and disease progression in patients with tuberculous pleural effusion.
abstract: Soluble and membrane-bound programmed death ligand-1 (sPD-L1 and mPD-L1, respectively) have been demonstrated to participate in the immune suppression of non-small cell lung cancer. However, the contribution of sPD-L1 and mPD-L1 to immune regulation and disease progression in patients with pleural effusions remains unknown. The present study evaluated the levels of sPD-L1 and membrane-bound PD-1/PD-L1 in the peripheral blood and pleural effusions of patients with tuberculous pleural effusion (TPE), malignant pleural effusion (MPE) and non-tuberculous non-malignant pleural effusion (n-TB n-M). Furthermore, selected T lymphocytes and cluster of differentiation (CD)14+monocytes were co-cultured to investigate the potential effect of the PD-1/PD-L1 pathway in TPE. Levels of sPD-L1 and PD-L1 on CD14+monocytes were increased in the TPE group, as compared with the MPE and n-TB n-M groups. Furthermore, sPD-L1 levels and the expression levels of PD-L1 on CD14+monocytes were demonstrated to be positively correlated with interferon (IFN)-γ concentration in pleural effusions. Therefore, IFN-γ may increase the expression of PD-L1 on CD14+monocytesin vitro. Cell counting kit-8 analysis demonstrated that anti-PD-L1 antibody was able to partially reverse the proliferation of T lymphocytes in the co-culture system. The results of the present study indicated that sPD-L1 or mPD-L1 are associated with the immune regulation and disease progression of TPE, and may serve as possible biomarkers of TPE. Furthermore, sPD-L1 and the PD-1/PD-L1 pathway of TPE may be associated with the Th1 immune response; therefore, an anti-PD-1/PD-L1 pathway suggests a potential immune therapy strategy for the treatment of TPE.
authors.affiliation: Department of Respiration, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215004, P.R. China.
authors.forename: Xue
authors.initials: X
authors.lastname: Pan
authors.affiliation: Department of Respiration, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215004, P.R. China.
authors.forename: Anyuan
authors.initials: A
authors.lastname: Zhong
authors.affiliation: Department of Respiration, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215004, P.R. China.
authors.forename: Yufei
authors.initials: Y
authors.lastname: Xing
authors.affiliation: Department of Respiration, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215004, P.R. China.
authors.forename: Minhua
authors.initials: M
authors.lastname: Shi
authors.affiliation: Department of Respiration, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215004, P.R. China.
authors.forename: Bin
authors.initials: B
authors.lastname: Qian
authors.affiliation: Department of Respiration, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215004, P.R. China.
authors.forename: Tong
authors.initials: T
authors.lastname: Zhou
authors.affiliation: Department of Immunology, Medical College of Soochow University, Suzhou, Jiangsu 215006, P.R. China; Key Laboratory of Infection and Immunity, Soochow University, Suzhou, Jiangsu 200241, P.R. China.
authors.forename: Yongjing
authors.initials: Y
authors.lastname: Chen
authors.affiliation: Department of Immunology, Medical College of Soochow University, Suzhou, Jiangsu 215006, P.R. China; Key Laboratory of Infection and Immunity, Soochow University, Suzhou, Jiangsu 200241, P.R. China.
authors.forename: Xueguang
authors.initials: X
authors.lastname: Zhang
keywords: antibody; interferon-γ; programmed death ligand-1; soluble programmed death ligand-1; tuberculous pleural effusion