title: Synergistic effects of alpha-1,2-fucosyltransferase, DAF, and CD59 in suppression of xenogenic immunological responses.
abstract: BACKGROUND
  Previous studies showed that alpha-1,2-fucosyltransferase (HT), decay accelerating factor (DAF), and CD59 have an inhibitory effect on the immunological rejection of xenogenic transplantation.
  
  
  METHODS
  To investigate their possible synergistic effects in suppression of heterogeneic transplantation, we produced transgenic mouse lines expressing human HT, DAF, and/or CD59 by the standard pronuclear injection approach. PCR and Southern blot were used to identify the transgenic founder lines. Flow cytometry confirmed the high-level expression of HT, DAF, or CD59 in the transgenic mice.
  
  
  RESULTS
  The deposition of IgM, C3c, or C9 in the cardiac vascular endothelial cells of the HT, HT/CD59, and/or DAF multiple positive transgenic mice was markedly decreased. The survival time and function of the hearts of the co-transgenic mice were significantly longer and higher than that of the single HT-positive transgenic mice (P < 0.05).
  
  
  CONCLUSIONS
  The mice co-expressing HT/DAF or HT/CD59 could resist the hyperacute rejection better than those expressing HT alone. It is feasible to use HT and C-reactive proteins co-transgenic tissues to resist hyperacute rejection and xenograft rejection.
authors.affiliation: Tianjin Institute of Urology and Second Hospital of Tianjin Medical University, Tianjin, China.
authors.forename: Sheng-Zhi
authors.initials: SZ
authors.lastname: Li
authors.forename: Yan-Chun
authors.initials: YC
authors.lastname: Qu
authors.forename: Bing-Qian
authors.initials: BQ
authors.lastname: Liu
authors.forename: Guang-You
authors.initials: GY
authors.lastname: Wang
authors.forename: Yue
authors.initials: Y
authors.lastname: Zhang
authors.forename: Zhi-Fang
authors.initials: ZF
authors.lastname: Ma
authors.forename: Teng-Xiang
authors.initials: TX
authors.lastname: Ma
authors.forename: Mengsheng
authors.initials: M
authors.lastname: Qiu
authors.forename: Rui-Fa
authors.initials: RF
authors.lastname: Han
mesh_terms: D000818:Animals; D000910:Antibodies, Heterophile / Q000378:metabolism*; D018958:CD55 Antigens / Q000235:genetics / Q000378:metabolism*; D018957:CD59 Antigens / Q000235:genetics / Q000378:metabolism*; D015932:Complement C3c / Q000378:metabolism; D003186:Complement C9 / Q000378:metabolism; D004730:Endothelium, Vascular / Q000276:immunology; D005647:Fucosyltransferases / Q000235:genetics / Q000378:metabolism*; D006084:Graft Rejection / Q000276:immunology / Q000517:prevention & control; D016027:Heart Transplantation / Q000276:immunology*; D006801:Humans; D007075:Immunoglobulin M / Q000378:metabolism; D051379:Mice; D008822:Mice, Transgenic; D009206:Myocardium / Q000276:immunology; D014183:Transplantation, Heterologous / Q000276:immunology*
chemical_list: D000910:Antibodies, Heterophile; D018958:CD55 Antigens; D018957:CD59 Antigens; D003186:Complement C9; D007075:Immunoglobulin M; D015932:Complement C3c; D005647:Fucosyltransferases