Evidence map›Paper›PMID 31534221›Full record

ArticleNature2019

FPR1 is the plague receptor on host immune cells.

Patrick Osei-Owusu, Thomas M Charlton, Hwan Keun Kim, Dominique Missiakas, Olaf Schneewind

Abstract read
In one paragraph

Article in Nature, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
12.9field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

40 citing papers in PubMed, 83 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Anti-infective compounds forSustainable microbiology · 2026
    Review
  5. FPR1-dependent Pro-inflammatory Ccl4Respiratory research · 2025
    Article
  6. Article
  7. Discovery ofActa pharmaceutica Sinica. B · 2025
    Article
  8. Article
  9. Article
  10. TheFrontiers in immunology · 2025
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Zoonoses (Shannon, Ireland) · 2023
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Patrick Osei-Owusu *Howard Taylor Ricketts Laboratory, Argonne National Laboratory, Lemont, IL, USA.
Thomas M Charlton *Howard Taylor Ricketts Laboratory, Argonne National Laboratory, Lemont, IL, USA.
Hwan Keun KimHoward Taylor Ricketts Laboratory, Argonne National Laboratory, Lemont, IL, USA.
Dominique MissiakasHoward Taylor Ricketts Laboratory, Argonne National Laboratory, Lemont, IL, USA. dmissiak@bsd.uchicago.edu.
Olaf SchneewindHoward Taylor Ricketts Laboratory, Argonne National Laboratory, Lemont, IL, USA.
Argonne National Laboratory · USUniversity of Chicago · US

Funding

Vaccines and Therapies Against BotulismU54AI057153 · NIAID · UNIVERSITY OF CHICAGO · PI SCHNEEWIND, OLAF · 2003 to 2013
$87.6M
Technology CoreU19AI107792 · NIAID · UNIVERSITY OF CHICAGO · PI CROSSON, SEAN · 2013 to 2017
$4.3M
Yersinia Type III Transport of Yop Proteins into Immune CellsR01AI042797 · NIAID · UNIVERSITY OF CHICAGO · PI SCHNEEWIND, OLAF · 1998 to 2013
$4.3M
NIAID NIH HHS R01 AI042797NIAID NIH HHS U19 AI107792NIAID NIH HHS U54 AI057153
6 · The paper itself

Abstract

The causative agent of plague, Yersinia pestis, uses a type III secretion system to selectively destroy immune cells in humans, thus enabling Y. pestis to reproduce in the bloodstream and be transmitted to new hosts through fleabites. The host factors that are responsible for the selective destruction of immune cells by plague bacteria are unknown. Here we show that LcrV, the needle cap protein of the Y. pestis type III secretion system, binds to the N-formylpeptide receptor (FPR1) on human immune cells to promote the translocation of bacterial effectors. Plague infection in mice is characterized by high mortality; however, Fpr1-deficient mice have increased survival and antibody responses that are protective against plague. We identified FPR1

Indexed as

AllelesAnimalsAntigens, BacterialBacterial AdhesionChemotaxisCRISPR-Cas SystemsDisease Models, AnimalFemaleHEK293 CellsHumansMacrophagesMaleMiceMice, Inbred C57BLNeutrophilsPlagueAntigens, BacterialFPR1 protein, humanFpr1 protein, mouseLcrV protein, YersiniaPore Forming Cytotoxic ProteinsReceptors, Formyl PeptideType III Secretion Systems

Identifiers

PMID31534221
PMCPMC6776691
OpenAlexW2973989845

What OpenQuestion holds

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LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.