title: Graft vasculopathy and tolerance: does the balance of Th cells contribute to graft vasculopathy?
abstract: BACKGROUND
  Cardiac allograft vasculopathy (CAV) is sometimes observed even though the allograft may survive indefinitely. In this study, we examined whether or not the preferential activation of Th2-type cells prevents the development of CAV.
  
  
  METHODS
  Hearts from C57BL/10 mice were transplanted heterotopically into the abdominal cavities of C3H.He recipient mice, and monoclonal antibodies (mAbs) to T-cell receptor (TCR) alphabeta or CD80/CD86 were administered after transplantation. The incidence of CAV was then examined histologically. To investigate the relative Th1/Th2 balance, the levels of IFNgamma and IL4 in the transplanted hearts were measured.
  
  
  RESULTS
  Indefinite heart graft survival was observed in mice treated with either the anti-TCRalphabeta or anti-CD80/CD86 mAbs and these mice accepted donor-type (C57BL/10) skin grafts but rejected those from a third party (BALB/c). Evidence of CAV was found in the mice treated with the anti-TCRalphabeta mAb, but CAV did not develop in the mice treated with anti-CD80/CD86 mAbs. Preferential activation of Th2-type cells was dominant in the tolerant mice treated with anti-TCRalphabeta mAb, but it was not dominant in the tolerant mice treated with anti-CD80/CD86 mAbs.
  
  
  CONCLUSIONS
  These findings suggest that the dominance of Th2-type cells does not prevent allograft vasculopathy.
authors.affiliation: First Department of Surgery, Yamaguchi University School of Medicine, Minamikogushi, Ube, Yamaguchi, 755-8505, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Hamano
authors.forename: H
authors.initials: H
authors.lastname: Bashuda
authors.forename: H
authors.initials: H
authors.lastname: Ito
authors.forename: B
authors.initials: B
authors.lastname: Shirasawa
authors.forename: K
authors.initials: K
authors.lastname: Okumura
authors.forename: K
authors.initials: K
authors.lastname: Esato
mesh_terms: D019264:Adoptive Transfer; D000818:Animals; D015703:Antigens, CD / Q000502:physiology; D018122:B7-1 Antigen / Q000502:physiology; D051940:B7-2 Antigen; D003324:Coronary Artery Disease / Q000209:etiology*; D006085:Graft Survival; D016027:Heart Transplantation / Q000009:adverse effects*; D007371:Interferon-gamma / Q000032:analysis; D015847:Interleukin-4 / Q000032:analysis; D008213:Lymphocyte Activation; D008297:Male; D008562:Membrane Glycoproteins / Q000502:physiology; D051379:Mice; D008807:Mice, Inbred BALB C; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D009206:Myocardium / Q000473:pathology; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000502:physiology; D018418:Th2 Cells / Q000502:physiology*; D014184:Transplantation, Homologous
chemical_list: D015703:Antigens, CD; D018122:B7-1 Antigen; D051940:B7-2 Antigen; C497965:Cd86 protein, mouse; D008562:Membrane Glycoproteins; D016693:Receptors, Antigen, T-Cell, alpha-beta; D015847:Interleukin-4; D007371:Interferon-gamma