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FPR1 is the plague receptor on host immune cells

Patrick Osei-Owusu1,2, Thomas M Charlton1,2, Hwan Keun Kim1,2

  • 1Howard Taylor Ricketts Laboratory, Argonne National Laboratory, Lemont, IL, USA.

Nature
|September 20, 2019
PubMed

Insights

Plague bacteria (Yersinia pestis) use a specific protein (LcrV) to target immune cells via the N-formylpeptide receptor (FPR1). Blocking or mutating FPR1 protects against plague, suggesting a role in host defense.

Area of Science:

  • Immunology
  • Microbiology
  • Genetics

Background:

  • Yersinia pestis causes plague by destroying immune cells using a type III secretion system.
  • The specific host factors mediating this immune cell destruction were previously unknown.

Purpose of the Study:

  • To identify the host receptor targeted by Y. pestis during infection.
  • To investigate the role of this receptor in plague pathogenesis and host survival.

Main Methods:

  • Investigated the interaction between Y. pestis LcrV protein and human immune cells.
  • Utilized Fpr1-deficient mice to assess survival and immune responses to plague.
  • Screened human populations for genetic variations in FPR1.

Main Results:

  • LcrV binds to the N-formylpeptide receptor (FPR1) on human immune cells, facilitating bacterial effector delivery.
  • Fpr1-deficient mice exhibited increased survival and protective antibody responses against plague.
  • Identified a human FPR1 variant (FPR1R190W) conferring resistance to Y. pestis-mediated immune cell destruction.

Conclusions:

  • FPR1 acts as a crucial receptor for Y. pestis in both mice and humans.
  • FPR1 deficiency or specific mutations provide significant protection against plague.
  • Plague has likely influenced the evolution of FPR1 alleles, impacting human immunity to other diseases.

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