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Identification of an H2-M3-restricted Listeria epitope: implications for antigen presentation by M3

L L Lenz1, B Dere, M J Bevan

  • 1Department of Immunology, University of Washington, Seattle, 98195, USA.

Immunity
|July 1, 1996
PubMed

Insights

Researchers identified a specific peptide from Listeria monocytogenes that effectively triggers CD8+ cytotoxic T cells. This N-formylated hexapeptide is crucial for immune response against this intracellular bacterial pathogen.

Area of Science:

  • Immunology
  • Microbiology
  • Molecular Biology

Background:

  • Intracellular bacterial pathogens like Listeria monocytogenes pose significant challenges to the host immune system.
  • Understanding the mechanisms of antigen presentation is key to developing effective immune responses.

Purpose of the Study:

  • To identify and characterize a specific epitope from Listeria monocytogenes recognized by H2-M3 restricted T cells.
  • To elucidate the role of peptide formylation in T cell activation and antigen presentation.

Main Methods:

  • Expression cloning was employed to identify the H2-M3-restricted epitope.
  • Synthetic peptides, including an N-formylated hexapeptide (fMIGWII), were synthesized and tested for T cell activation.
  • Bioinformatic analysis of the epitope's source protein sequence and predicted membrane topology.

Main Results:

  • An N-formylated hexapeptide, fMIGWII, from Listeria monocytogenes was identified as a potent H2-M3-restricted epitope.
  • Picomolar concentrations of the formylated peptide induced significant CD8+ cytotoxic T cell lysis.
  • The non-formylated peptide showed a 100-fold lower activity, highlighting the importance of N-formylation.
  • The epitope originates from a predicted transmembrane protein with an N(out)-C(in) topology, protecting it from bacterial deformylases.

Conclusions:

  • The N-formylated hexapeptide fMIGWII is a critical determinant for H2-M3-restricted CD8+ T cell recognition of Listeria monocytogenes.
  • The unique membrane topology of the epitope's source protein explains its protection from bacterial enzymes and suggests a vacuolar, TAP-independent antigen presentation pathway in phagocytes.

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