title: Inhibition of arterial allograft intimal hyperplasia using recipient dendritic cells pretreated with B7 antisense peptide.
abstract: BACKGROUND
  Low expression or absence of dendritic cell (DC) surface B7 molecules can induce immune tolerance or hyporesponse. Whether DCs could induce indirect allogeneic-specific cross-tolerance or hyporesponse to recipient T cells remains unclear.
  
  
  METHODS
  Generated from C3H/He mice bone marrow cells pulsed with donor antigen from C57BL/6 mice, recipient DCs were incubated with B7 antisense peptide (B7AP). Immune regulatory activities were examined in vitro by a series of mixed lymphocyte reactions. Murine allogeneic carotid artery orthotopic transplantation was performed from C57BL/6 to C3H/He. Recipients were given B7AP-treated DCs 7 days before transplantation. Allograft pathological analysis was done 2 months after transplantation.
  
  
  RESULTS
  B7AP-pretreated DCs markedly inhibited T-cell proliferation compared with untreated group. Pretreated T cells exhibited markedly reduced response to alloantigen versus third-party antigen. Pathological analysis of arterial allografts demonstrated significant reduction of intimal hyperplasia in B7-AP pretreated group versus control.
  
  
  CONCLUSIONS
  Blockade of B7 molecules by B7AP could induce indirect allogeneic-specific hyporesponse and inhibit arterial allograft intimal hyperplasia, which may be involved in future strategies for human allograft chronic rejection.
authors.affiliation: Department of General Surgery, Huashan Hospital, Fudan University, Shanghai 200040, China.
authors.forename: Yu-Feng
authors.initials: YF
authors.lastname: Yao
authors.forename: Yi-Ming
authors.initials: YM
authors.lastname: Zhou
authors.forename: Jian-Bin
authors.initials: JB
authors.lastname: Xiang
authors.forename: Xiao-Dong
authors.initials: XD
authors.lastname: Gu
authors.forename: Duan
authors.initials: D
authors.lastname: Cai
mesh_terms: D000818:Animals; D060887:B7 Antigens / Q000276:immunology; D002339:Carotid Arteries / Q000276:immunology / Q000637:transplantation*; D002450:Cell Communication; D049109:Cell Proliferation; D003713:Dendritic Cells / Q000187:drug effects / Q000276:immunology* / Q000637:transplantation; D006084:Graft Rejection / Q000276:immunology / Q000517:prevention & control*; D006085:Graft Survival / Q000276:immunology; D006801:Humans; D006965:Hyperplasia / Q000517:prevention & control*; D007108:Immune Tolerance; D008213:Lymphocyte Activation; D007959:Lymphocyte Culture Test, Mixed; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D010455:Peptides / Q000276:immunology / Q000494:pharmacology*; D013601:T-Lymphocytes / Q000276:immunology; D014184:Transplantation, Homologous
chemical_list: D060887:B7 Antigens; D010455:Peptides