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Immunologic tolerance: tailored antigen

A M Krensky1, C Clayberger

  • 1Department of Pediatrics, Stanford University School of Medicine, CA 94305-5119, USA.

Transplantation Proceedings
|August 1, 1996
PubMed
Summary
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Synthetic HLA peptides inhibit T-cell responses by binding heat shock proteins, inducing tolerance. This interaction increases intracellular calcium and down-regulates NF-AT, suggesting a novel immunophilin role for heat shock proteins in T-cell anergy.

Area of Science:

  • Immunology
  • Molecular Biology

Background:

  • Heat shock proteins (HSPs) are involved in protein folding and trafficking.
  • HSPs can bind exogenous drugs, similar to known immunophilins like cyclophilins and FK 506 binding proteins.
  • Immunophilins mediate immunosuppressive effects of drugs like cyclosporine and FK 506 by interacting with calcineurin.

Purpose of the Study:

  • To investigate the mechanism by which synthetic peptides of HLA class I molecules inhibit T-cell responses.
  • To explore the potential role of heat shock proteins as novel immunophilins.
  • To elucidate the pathways leading to T-cell anergy induced by synthetic HLA peptides.

Main Methods:

  • Synthetic peptides corresponding to linear sequences of HLA class I molecules were used.
  • In vitro and in vivo T-cell responses were measured.

Related Experiment Videos

  • Intracellular calcium levels and nuclear factor of activated T cells (NF-AT) regulation were assessed.
  • Binding interactions between peptides and heat shock proteins were investigated.

    • Main Results:

    • Synthetic HLA peptides were found to inhibit T-cell responses.
    • These peptides induce immunologic tolerance through binding to heat shock protein 70 (hsp-70) family members.
    • Peptide binding to hsp-70 increased intracellular calcium and down-regulated NF-AT.
    • This suggests heat shock proteins may function as novel immunophilins.

    Conclusions:

    • Synthetic HLA peptides can induce immunologic tolerance by modulating T-cell activation pathways.
    • Heat shock proteins may act as novel immunophilins, mediating the immunosuppressive effects of these peptides.
    • Peptide binding to heat shock proteins disrupts normal T-cell activation, leading to a persistent state of anergy.