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⇱ Concerted peptide trimming by human ERAP1 and ERAP2 aminopeptidase complexes in the endoplasmic reticulum | Nature Immunology


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Abstract

The generation of many HLA class I peptides entails a final trimming step in the endoplasmic reticulum that, in humans, is accomplished by two 'candidate' aminopeptidases. We show here that one of these, ERAP1, was unable to remove several N-terminal amino acids that were trimmed efficiently by the second enzyme, ERAP2. This trimming of a longer peptide required the concerted action of both ERAP1 and ERAP2, both for in vitro digestion and in vivo for cellular antigen presentation. ERAP1 and ERAP2 localized together in vivo and associated physically in complexes that were most likely heterodimeric. Thus, the human endoplasmic reticulum is equipped with a pair of trimming aminopeptidases that have complementary functions in HLA class I peptide presentation.

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Figure 1: Multiple aminopeptidase activities are associated with human B cell microsomes.
The alternative text for this image may have been generated using AI.
Figure 2: ERAP1 and ERAP2 localize together in the ER.
The alternative text for this image may have been generated using AI.
Figure 3: ERAP1 and ERAP2 form ER-resident complexes.
The alternative text for this image may have been generated using AI.
Figure 4: Specific and cooperative peptide trimming by ERAP1 and ERAP2.
The alternative text for this image may have been generated using AI.
Figure 5: Effect of ERAP knockdown on HLA class I expression and epitope presentation.
The alternative text for this image may have been generated using AI.

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Acknowledgements

We thank Y. Samino for env-specific CTLs and for the purification of env-derived synthetic peptides. Supported by the European Commission (QLK2-CT-2001-01167 to P.M.v.E., F.G. and G.N), Comunidad de Madrid and Fundación para la Investigación y Prevención del Síndrome de Immunodeficiencia Adquirita en Espana (D.L.), Ministerio de Educación y Ciencia and Red Temática de Investigación Cooperativa en Síndrome de Immunodeficiencia Adquirita del Fondo de Investigaciónes Sanitarias (M.D.V.), Fondation pour la Recherche Médicale (D.F.), Institut National de la Santé et de la Recherche Médicale (O.C.) and K. Bauer (MPI Hannover, Germany; L. Schomburg).

Author information

Author notes
  1. Doriana Fruci

    Present address: Research Center Ospedale Bambino Gesù, 00165, Rome, Italy

  2. Gabriele Niedermann

    Present address: Clinic of Radiation Oncology, Experimental Division, University Clinic, Freiburg, Germany

Authors and Affiliations

  1. Institut National de la Sante et Recherche Médicale Unité, 580

    Loredana Saveanu, Oliver Carroll, Doriana Fruci & Peter M van Endert

  2. Université René Descartes Paris 5, Paris, 75015, France

    Loredana Saveanu, Oliver Carroll, Doriana Fruci & Peter M van Endert

  3. M-SCAN, Fishponds Close, Wokingham, RG41 2TZ, Berkshire, UK

    Vivian Lindo & Fiona Greer

  4. Centro Nacional de Microbiología, Instituto de Salud Carlos III, Majadahonda, 28220, Spain

    Margarita Del Val & Daniel Lopez

  5. Centre National de la Recherche Scientifique UMR 8147, Necker Institute, Paris, 75015, France

    Yves Lepelletier

  6. Institut für Experimentelle Endokrinologie, Charité-Universitätsmedizin Berlin, Berlin, 10117, Germany

    Lutz Schomburg

  7. Max-Planck Institut für Immunbiologie, Freiburg, 79108, Germany

    Gabriele Niedermann

Authors
  1. Loredana Saveanu
  2. Oliver Carroll
  3. Vivian Lindo
  4. Margarita Del Val
  5. Daniel Lopez
  6. Yves Lepelletier
  7. Fiona Greer
  8. Lutz Schomburg
  9. Doriana Fruci
  10. Gabriele Niedermann
  11. Peter M van Endert

Corresponding author

Correspondence to Peter M van Endert.

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Competing interests

The authors declare no competing financial interests.

Supplementary information

Supplementary Table 1 (download PDF )

Oligonucleotides used for ERAP1 and ERAP2 knockdown (PDF 28 kb)

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Saveanu, L., Carroll, O., Lindo, V. et al. Concerted peptide trimming by human ERAP1 and ERAP2 aminopeptidase complexes in the endoplasmic reticulum. Nat Immunol 6, 689–697 (2005). https://doi.org/10.1038/ni1208

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  • DOI: https://doi.org/10.1038/ni1208

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