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Acute rejection of vascular heart allografts by perforin‐deficient mice
Author(s) -
Schulz Manfred,
Schuurman HenkJan,
Joergensen Joanne,
Steiner Carolina,
Meerloo Timo,
Kägi David,
Hengartner Hans,
Zinkernagel Rolf M.,
Schreier Max H.,
Bürki Kurt,
Ledermann Birgit
Publication year - 1995
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.1830250225
Subject(s) - perforin , biology , cd8 , immunology , effector , cytotoxic t cell , peripheral blood mononuclear cell , heart transplantation , t cell , histocompatibility , flow cytometry , t lymphocyte , lymphocyte , transplantation , antigen , immune system , human leukocyte antigen , in vitro , medicine , biochemistry
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 cellmediated 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).