title: Overexpression of programmed death-1 ligand-1 on NIT cells lead to negative regulation of allogeneic lymphocyte activation.
abstract: PD-L1 have been identified as the ligand for PD-1, and shown to play a role in the regulation of immune responses. In the present study, we investigated whether overexpressing PD-L1 on islet beta cells could induce negative regulation in primary and primed allogeneic lymphocyte response. pPD-L1-EGFP or pEGFPn1 were transfected in NIT-1 cells, for establishment of pPD-L1-EGFP or pEGFPn1 stable transfectants, namely NIT-PD-L1 and NIT-EGFP. In mixed cells reaction, as compared with the controls of NIT-1 or NIT-EGFP, NIT-PD-L1-primed splenocytes showed the lowest proliferative response but severe apoptosis when restimulated with NIT-PD-L1 cells in vitro. Overexpressing PD-L1 on NIT-1 cells could downregulate IFN-gamma but upregulate IL-4 and IL-10 production by the primed lymphocytes. In addition, proliferative response of primary reactive lymphocytes stimulated with NIT-PD-L1 was lower than those lymphocytes restimulated with NIT-1 cells or NIT-EGFP cells. Our data demonstrated that PD-L1 has down-regulative effects on alloimmune responses.
authors.affiliation: Department of Neurosurgery, Wuhan General Hospital of Guangzhou Command, Wuhan 430070, China.
authors.forename: Xue
authors.initials: X
authors.lastname: Wen
authors.forename: Guozheng
authors.initials: G
authors.lastname: Xu
authors.forename: Jing
authors.initials: J
authors.lastname: Liu
authors.forename: Huifen
authors.initials: H
authors.lastname: Zhu
authors.forename: Hong
authors.initials: H
authors.lastname: Dai
authors.forename: Li
authors.initials: L
authors.lastname: Li
authors.forename: Yi
authors.initials: Y
authors.lastname: Hong
authors.forename: Jing
authors.initials: J
authors.lastname: Yang
authors.forename: Wei
authors.initials: W
authors.lastname: Dai
authors.forename: Lei
authors.initials: L
authors.lastname: Ping
authors.forename: Guanxin
authors.initials: G
authors.lastname: Shen
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000096:biosynthesis / Q000235:genetics* / Q000276:immunology; D017209:Apoptosis / Q000276:immunology; D060890:B7-H1 Antigen; D002460:Cell Line; D049109:Cell Proliferation; D016207:Cytokines / Q000096:biosynthesis* / Q000235:genetics; D015536:Down-Regulation / Q000276:immunology; D025461:Feedback, Physiological; D006801:Humans; D007114:Immunization; D050417:Insulin-Secreting Cells / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D008213:Lymphocyte Activation; D007959:Lymphocyte Culture Test, Mixed; D051379:Mice; D008807:Mice, Inbred BALB C; D050378:T-Lymphocytes, Regulatory / Q000276:immunology; D019076:Transgenes / Q000235:genetics; D014184:Transplantation, Homologous
chemical_list: D015703:Antigens, CD; D060890:B7-H1 Antigen; C423236:CD274 protein, human; D016207:Cytokines