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Puromycin-sensitive aminopeptidase limits MHC class I presentation in dendritic cells but does not affect CD8 T cell responses during viral infections.

Previous experiments using enzyme inhibitors, cell lysates, and purified enzyme have suggested that puromycin-sensitive aminopeptidase (PSA) plays a role in creating and destroying MHC class I-presented peptides although its precise contribution to these processes is unknown. To examine the importance of this enzyme in MHC class I Ag presentation, we have generated PSA-deficient mice and cell lines from these animals. PSA-deficient mice are smaller and do not reproduce as well as wild type mice. In addition, dendritic cells from PSA-deficient mice display more MHC class I molecules on the cell surface, suggesting that PSA normally limits Ag presentation by destroying certain peptides in these key APCs. Surprisingly, MHC class I levels are not altered on other PSA-deficient cells and the processing and presentation of peptide precursors in PSA-deficient fibroblasts is normal. Moreover, PSA-deficient mice have normal numbers of T cells in the periphery, and respond as well as wild type mice to eight epitopes from three viruses. These data indicate that PSA may play a role in limiting MHC class I Ag presentation in dendritic cells in vivo but that it is not essential for generating most MHC class I-presented peptides or for stimulating CTL responses to several Ags.

Pubmed ID: 18209067


  • Towne CF
  • York IA
  • Neijssen J
  • Karow ML
  • Murphy AJ
  • Valenzuela DM
  • Yancopoulos GD
  • Neefjes JJ
  • Rock KL


Journal of immunology (Baltimore, Md. : 1950)

Publication Data

February 1, 2008

Associated Grants

  • Agency: NIAID NIH HHS, Id: AI 07349
  • Agency: NIDDK NIH HHS, Id: DK 42520

Mesh Terms

  • Amino Acid Sequence
  • Aminopeptidases
  • Animals
  • Antigen Presentation
  • Antigens, Viral
  • CD8-Positive T-Lymphocytes
  • Dendritic Cells
  • Epitopes
  • Histocompatibility Antigens Class I
  • Mice
  • Mice, Mutant Strains
  • Molecular Sequence Data
  • Peptides
  • Virus Diseases
  • Viruses