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Elife. 2015 Oct 6;4. pii: e09617. doi: 10.7554/eLife.09617.

TAPBPR alters MHC class I peptide presentation by functioning as a peptide exchange catalyst.

Author information

1
Department of Pathology, University of Cambridge, Cambridge, United Kingdom.
2
Faculty of Medicine and Institute for Life Science, University of Southampton, Southampton, United Kingdom.
3
Department of Immunology, Eberhard Karls University Tübingen, Tübingen, Germany.
4
Cancer Research UK Protein Core Facility, Faculty of Medicine, University of Southampton, Southampton, United Kingdom.
5
Cambridge Institute for Medical Research, University of Cambridge, Cambridge, United Kingdom.

Abstract

Our understanding of the antigen presentation pathway has recently been enhanced with the identification that the tapasin-related protein TAPBPR is a second major histocompatibility complex (MHC) class I-specific chaperone. We sought to determine whether, like tapasin, TAPBPR can also influence MHC class I peptide selection by functioning as a peptide exchange catalyst. We show that TAPBPR can catalyse the dissociation of peptides from peptide-MHC I complexes, enhance the loading of peptide-receptive MHC I molecules, and discriminate between peptides based on affinity in vitro. In cells, the depletion of TAPBPR increased the diversity of peptides presented on MHC I molecules, suggesting that TAPBPR is involved in restricting peptide presentation. Our results suggest TAPBPR binds to MHC I in a peptide-receptive state and, like tapasin, works to enhance peptide optimisation. It is now clear there are two MHC class I specific peptide editors, tapasin and TAPBPR, intimately involved in controlling peptide presentation to the immune system.

KEYWORDS:

MHC; antigen processing and presentation; cell biology; human; immunology; peptide repertoire

PMID:
26439010
PMCID:
PMC4718805
DOI:
10.7554/eLife.09617
[Indexed for MEDLINE]
Free PMC Article

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