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Human CD45 is an F-component-specific receptor for the staphylococcal toxin Panton-Valentine leukocidin

Angelino T Tromp1, Michiel Van Gent1,2, Pauline Abrial3

  • 1Department of Medical Microbiology, University Medical Center Utrecht, Utrecht, The Netherlands.

Nature Microbiology
|May 9, 2018
PubMed

Insights

Staphylococcal leukocidins target human immune cells. Researchers found the toxin component LukF-PV binds to CD45, explaining why mouse immune cells resist Panton-Valentine leukocidin (PVL) during infection.

Area of Science:

  • Microbiology
  • Immunology
  • Molecular Biology

Background:

  • Staphylococcal bi-component leukocidins, Panton-Valentine leukocidin (PVL) and γ-haemolysin CB (HlgCB), target human phagocytes.
  • The S-components of these toxins bind to human complement C5a receptor 1 (C5aR1), contributing to their cellular tropism and human specificity.

Purpose of the Study:

  • To investigate the role of PVL and HlgCB during infection using a human C5aR1 knock-in (hC5aR1KI) mouse model.
  • To elucidate the molecular mechanisms underlying the differential sensitivity of human and murine phagocytes to PVL.

Main Methods:

  • Development of a human C5aR1 knock-in (hC5aR1KI) mouse model.
  • Infection studies in hC5aR1KI mice to assess bacterial loads.
  • Genome-wide CRISPR-Cas9 screening to identify PVL receptors.

Main Results:

  • HlgCB, but not PVL, increased bacterial loads in hC5aR1KI mice.
  • Murine hC5aR1KI neutrophils exhibited reduced sensitivity to PVL, mediated by the F-component LukF-PV.
  • CD45 was identified as a receptor for LukF-PV, explaining the resistance of mouse neutrophils to PVL.

Conclusions:

  • The human-specific interaction between LukF-PV and CD45 provides a molecular basis for PVL resistance in mouse neutrophils.
  • The F-component plays a critical, previously unsuspected role in determining phagocyte sensitivity to PVL.
  • This study highlights the importance of the F-component in PVL's mechanism of action against human immune cells.

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