title: Molecular Chimeric Recipient Precursor T Cells Promote Cardiac Allograft Survival in Mice.
abstract: BACKGROUND
  Molecular chimerism has become a potential method to induce donor-specific transplant tolerance. We researched the prolongation of cardiac allograft survival by recipient mouse molecular chimeric precursor T cells (pre-T cells) or hematopoietic stem cells (HSCs) infusion in vivo.
  
  
  METHODS
  The donor C57BL/6 mouse MHC-I gene (H-2K(b) and H-2D(b) gene) were amplified by RT-PCR. The identified recipient BALB/c mouse pre-T cells and HSCs were transduced by the pMSCVneo retroviral vector of C57BL/6 mouse MHC-I gene (pMSCVneo-H-2D(b)/H-2K(b)). Then the molecular chimeric cells were transfused back to the BALB/c mice. Allogeneic T-lymphocyte proliferation was assessed in mixed lymphocyte reactions (MLR). A mouse model of heterotopic abdominal heart transplantation was performed to evaluate survival times and histological grade of acute rejection at 7 days after transplantation.
  
  
  RESULTS
  BALB/c mice molecular chimeric pre-T cells and HSCs were cultured successfully after pMSCV-H-2D(b)/H-2K(b) transduction. After the molecular chimeric pre-T cell treatment, the result of MLR showed that the stimulating index of allogeneic T lymphocyte had a statistically significant decrease, which also exhibited a significant reduction after molecular chimeric HSC treatment. The survival time of cardiac allograft was prolonged after chimeric pre-T cell or HSC infusion; meanwhile, pathologic rejection grade decreased significantly. Nevertheless, molecular chimeric pre-T cells exhibited a longer median survival time.
  
  
  CONCLUSIONS
  The molecular chimeric recipient mouse pre-T cell or HSC infusion reduced spleen T cells' response to allogeneic T cells in vitro and delayed cardiac allograft rejection in vivo. Pre-T cells have more advantages than HSCs on the prolongation of mouse cardiac allograft survival.
authors.affiliation: Department of General Surgery, Tianjin Medical University General Hospital, Tianjin, China.
authors.forename: L
authors.initials: L
authors.lastname: Lu
authors.affiliation: Department of General Surgery, Tianjin Medical University General Hospital, Tianjin, China.
authors.forename: G
authors.initials: G
authors.lastname: Zhang
authors.affiliation: Department of General Surgery, Tianjin Medical University General Hospital, Tianjin, China.
authors.forename: R
authors.initials: R
authors.lastname: Li
authors.affiliation: Department of General Surgery, Tianjin Medical University General Hospital, Tianjin, China.
authors.forename: Z
authors.initials: Z
authors.lastname: Zhao
authors.affiliation: Department of General Surgery, Tianjin Medical University General Hospital, Tianjin, China.
authors.forename: W
authors.initials: W
authors.lastname: Li
authors.affiliation: Department of General Surgery, Tianjin Medical University General Hospital, Tianjin, China.
authors.forename: T
authors.initials: T
authors.lastname: Liu
authors.affiliation: Department of General Surgery, Tianjin Medical University General Hospital, Tianjin, China. Electronic address: tjmughgs_fwh@163.com.
authors.forename: W
authors.initials: W
authors.lastname: Fu
mesh_terms: D064591:Allografts; D000818:Animals; D046528:Chimerism; D004195:Disease Models, Animal; D005260:Female; D006085:Graft Survival / Q000276:immunology*; D016027:Heart Transplantation; D007111:Immunity, Cellular; D008213:Lymphocyte Activation; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D013601:T-Lymphocytes / Q000276:immunology*; D066027:Transplant Recipients; D023001:Transplantation Tolerance / Q000276:immunology*