Long-Term Acceptance of Major Histocompatibility Complex-Mismatched Cardiac Allograft Induced by a Low Dose of CTLA4IgM Plus FK506

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  • YAMADA Akira
    Section of Immunopathogenesis, Institute of Immunological Science, Hokkaido University
  • MURAKAMI Masaaki
    Section of Immunopathogenesis, Institute of Immunological Science, Hokkaido University
  • IJIMA Kenichi
    Section of Immunopathogenesis, Institute of Immunological Science, Hokkaido University
  • YAGITA Hideo
    Department of Immunology, Juntendo University School of Medicine
  • OKUMURA Ko
    Department of Immunology, Juntendo University School of Medicine
  • KOMATSU Sakuzo
    Department of Surgery, Sapporo Medical University School of Medicine
  • UEDE Toshimitsu
    Section of Immunopathogenesis, Institute of Immunological Science, Hokkaido University

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The imnunosuppressant FK506 prolongs allograft survival. However, at therapeutic doses it has significant side effects. A fusion protein consisting of the extracellular portion of CTLA4 and the Fc portion of human IgG (CTLA4IgG) also prolongs allograft survival, but large doses of CTLA4IgG are required for the induction of cardiac allograft acceptance. Therefore, we constructed a pentameric form of a new CTLA4 fusion protein, CTLA4IgM. We tested whether low doses of CTLA4IgG or CTLA4IgM in combination with subtherapeutic doses of FK506 can prolong allograft survival in a synergistic fashion. C57BL/6 (H-2b) neonatal hearts were transplanted to CBA/J (H-2k) mice in a heterotopic, nonvascularized cardiac allograft model. The findings demonstrate that a combination of low doses of FK506 plus a pentameric form of CTLA4Ig, CTLA4IgM, leads to significant graft survival, while a combination of FK506 plus CTLA4IgG does not.

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