Donor-derived soluble MHC antigens plus low-dose cyclosporine induce transplantation unresponsiveness independent of the thymus by down-regulating T cell-mediated alloresponses in a rat transplantation model

Transplantation. 2001 Dec 27;72(12):1974-82. doi: 10.1097/00007890-200112270-00018.

Abstract

Background: In vitro, soluble MHC (sMHC) antigens modulate and induce apoptosis in alloreactive and antigen-specific T cells, demonstrating their potency to regulate T cell-mediated immune responses. However, their efficacy to regulate immunological responses in vivo remains unclear. Here, we report that repetitive intraperitoneal injection of recombinant Lewis rat-derived MHC class I antigens in Dark Agouti (DA) rats modulates alloreactivity.

Methods: RT1.A1 (Lewis derived) genes were cloned into mammalian expression vectors, and RT1.Aa (DA derived) genes were used to transfect a rat myeloma cell line. RT1.A1 molecules were injected intraperitoneally in DA recipients that subsequently underwent transplantation with Lewis-derived cardiac allografts.

Results: Soluble class I antigens were secreted by the transfected cells and were shown to be heterodimeric, peptide-loaded, and conformationally folded. Injection of donor-derived soluble MHC significantly reduced the ability of recipient animals to mount a cytotoxic T-cell response to donor-derived tissue. More interestingly, this treatment significantly prolonged donor-graft survival and allowed 60% of treated animals to develop graft tolerance (>120 days), when donor sMHC were combined with a single subtherapeutic dosage of cyclosporine. Thymectomy of recipient animals before transplantation did not interfere with induction of peripheral tolerance.

Conclusions: Donor-derived sMHC are potential tolerogens for down-regulating the cytotoxic T-cell response of animals that undergo transplantation. Thus, these data provide for the first time a rationale for the application of directly injected sMHC in vivo to down-regulate immunological responses and aid the induction of graft tolerance.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibody Formation
  • Apoptosis
  • CD4-Positive T-Lymphocytes / pathology
  • Cyclosporine / administration & dosage*
  • Cyclosporine / pharmacology
  • Dose-Response Relationship, Drug
  • Down-Regulation
  • Graft Survival / drug effects
  • Heart Transplantation / immunology*
  • Histocompatibility Antigens / metabolism
  • Histocompatibility Antigens Class I / pharmacology*
  • Immunosuppressive Agents / administration & dosage*
  • Immunosuppressive Agents / pharmacology
  • Isoantibodies / biosynthesis
  • Myocardium / pathology
  • Rats
  • Rats, Inbred Lew
  • Rats, Inbred Strains
  • T-Lymphocytes / drug effects
  • T-Lymphocytes / physiology*
  • T-Lymphocytes, Cytotoxic / drug effects
  • T-Lymphocytes, Cytotoxic / physiology
  • Thymus Gland / physiology
  • Tissue Donors*
  • Transfection
  • Transplantation Tolerance*
  • Tumor Cells, Cultured

Substances

  • Histocompatibility Antigens
  • Histocompatibility Antigens Class I
  • Immunosuppressive Agents
  • Isoantibodies
  • histocompatibility antigens RT, rat
  • Cyclosporine