Acute rejection of vascular heart allografts by perforin-deficient mice

Eur J Immunol. 1995 Feb;25(2):474-80. doi: 10.1002/eji.1830250225.

Abstract

To study the role of perforin in cell-mediated graft rejection, vascularized hearts were grafted to perforin-deficient C57BL/6 and control C57BL/6 recipient mice. Fully allogeneic heart grafts (BALB/c) were acutely rejected by both recipients within 6 days. Peritoneal exudate lymphocytes from control mice but not from perforin-deficient mice exhibit a strong alloreactive cytotoxic activity in vitro. Histological analysis of the rejected tissues demonstrated extensive mononuclear cell infiltrates in both recipients. Flow cytometry analysis and immunohistology of graft-infiltrating cells showed similar proportions of lymphocyte subsets (CD8 >> CD4). Collectively, these data indicate that perforin is not essential in the cell-mediated acute rejection of a fully mismatched heart allograft. However, perforin-dependent effector mechanisms appeared to be limiting in the T cell-mediated rejection of heart allografts differing only at a single major histocompatibility complex class I antigen (bm1), because these grafts survived longer (mean 87.8 days) in perforin-deficient than in control mice (mean 31.5 days).

MeSH terms

  • Animals
  • Antigens, Surface / physiology
  • Cytotoxicity, Immunologic
  • Graft Rejection*
  • Heart Transplantation / immunology*
  • Male
  • Membrane Glycoproteins / deficiency*
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C3H
  • Mice, Inbred C57BL
  • Myocardium / pathology
  • Perforin
  • Pore Forming Cytotoxic Proteins
  • T-Lymphocyte Subsets / immunology
  • Transplantation, Homologous
  • fas Receptor

Substances

  • Antigens, Surface
  • Membrane Glycoproteins
  • Pore Forming Cytotoxic Proteins
  • fas Receptor
  • Perforin