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Related Experiment Videos

Recent developments in MHC-class-I-mediated antigen presentation.

Paul J Lehner1, Peter Cresswell

  • 1Lab 5.19, Cambridge Institute for Medical Research, Addenbrooke's Hospital, Hills Rd, CB2 2XY Cambridge, UK. pjl30@cam.ac.uk

Current Opinion in Immunology
|January 22, 2004
PubMed
Summary
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Defective ribosomal products and phagosome biogenesis enable cross-presentation of antigens by antigen-presenting cells. Emerging viral E3 ligases also target MHC class I molecules for degradation.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cellular Biology

Background:

  • Defective ribosomal products (DRiPs) are a source of endogenous peptides for MHC class I antigen presentation.
  • Phagosome biogenesis recruits endoplasmic reticulum membrane, facilitating cytosolic translocation of exogenous antigens.
  • Specialized antigen-presenting cells utilize these mechanisms for cross-presentation.

Purpose of the Study:

  • To elucidate the mechanisms of cross-presentation involving DRiPs and phagosome biogenesis.
  • To highlight the role of viral ubiquitin E3 ligases in modulating MHC class I presentation.

Main Methods:

  • Analysis of endogenous peptide supply for MHC class I pathway.
  • Investigation of phagosome biogenesis and antigen translocation.

Related Experiment Videos

  • Characterization of K3 family viral ubiquitin E3 ligases.

    • Main Results:

    • DRiPs are a significant source of peptides for the MHC class I pathway.
    • Phagosome biogenesis provides access to cytosolic antigen processing and presentation machinery.
    • Viral K3 ligases constitutively degrade MHC class I molecules and immunoreceptors.

    Conclusions:

    • Combined mechanisms of DRiPs and phagosome biogenesis facilitate cross-presentation.
    • Viral E3 ligases represent a novel mechanism for immune evasion by targeting MHC class I.