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FPR1 is the plague receptor on host immune cells
by
Charlton, Thomas M.
, Osei-Owusu, Patrick
, Schneewind, Olaf
, Missiakas, Dominique
, Kim, Hwan Keun
in
13/106
/ 13/109
/ 13/31
/ 13/51
/ 14/19
/ 14/63
/ 631/250/255/1318
/ 631/326/421
/ 64/60
/ 82/29
/ 82/83
/ Alleles
/ Analysis
/ Animals
/ Antibodies
/ Antigens, Bacterial - metabolism
/ Bacteria
/ Bacterial Adhesion
/ Causes of
/ Cell receptors
/ Chemotaxis - immunology
/ CRISPR
/ CRISPR-Cas Systems
/ Destruction
/ Development and progression
/ Disease Models, Animal
/ Female
/ Gene expression
/ Genomes
/ HEK293 Cells
/ Human behavior
/ Humanities and Social Sciences
/ Humans
/ Immune response
/ Immune system
/ Infections
/ Infectious diseases
/ LcrV protein
/ Leukocytes (neutrophilic)
/ Macrophages - cytology
/ Macrophages - immunology
/ Macrophages - metabolism
/ Macrophages - microbiology
/ Male
/ Mice
/ Mice, Inbred C57BL
/ multidisciplinary
/ Mutation
/ Neoplasms
/ Neutrophils
/ Neutrophils - cytology
/ Neutrophils - immunology
/ Neutrophils - metabolism
/ Neutrophils - microbiology
/ Pandemics
/ Pathogens
/ Physiological aspects
/ Plague
/ Plague - immunology
/ Plague - microbiology
/ Plague - prevention & control
/ Plasmids
/ Polymorphism, Single Nucleotide - genetics
/ Pore Forming Cytotoxic Proteins - metabolism
/ Proteins
/ Receptors, Formyl Peptide - antagonists & inhibitors
/ Receptors, Formyl Peptide - deficiency
/ Receptors, Formyl Peptide - genetics
/ Receptors, Formyl Peptide - metabolism
/ Science
/ Science (multidisciplinary)
/ Translocation
/ Type III Secretion Systems - drug effects
/ U937 Cells
/ Vaccines
/ Yersinia pestis
/ Yersinia pestis - chemistry
/ Yersinia pestis - immunology
/ Yersinia pestis - metabolism
/ Yersinia pestis - pathogenicity
2019
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FPR1 is the plague receptor on host immune cells
by
Charlton, Thomas M.
, Osei-Owusu, Patrick
, Schneewind, Olaf
, Missiakas, Dominique
, Kim, Hwan Keun
in
13/106
/ 13/109
/ 13/31
/ 13/51
/ 14/19
/ 14/63
/ 631/250/255/1318
/ 631/326/421
/ 64/60
/ 82/29
/ 82/83
/ Alleles
/ Analysis
/ Animals
/ Antibodies
/ Antigens, Bacterial - metabolism
/ Bacteria
/ Bacterial Adhesion
/ Causes of
/ Cell receptors
/ Chemotaxis - immunology
/ CRISPR
/ CRISPR-Cas Systems
/ Destruction
/ Development and progression
/ Disease Models, Animal
/ Female
/ Gene expression
/ Genomes
/ HEK293 Cells
/ Human behavior
/ Humanities and Social Sciences
/ Humans
/ Immune response
/ Immune system
/ Infections
/ Infectious diseases
/ LcrV protein
/ Leukocytes (neutrophilic)
/ Macrophages - cytology
/ Macrophages - immunology
/ Macrophages - metabolism
/ Macrophages - microbiology
/ Male
/ Mice
/ Mice, Inbred C57BL
/ multidisciplinary
/ Mutation
/ Neoplasms
/ Neutrophils
/ Neutrophils - cytology
/ Neutrophils - immunology
/ Neutrophils - metabolism
/ Neutrophils - microbiology
/ Pandemics
/ Pathogens
/ Physiological aspects
/ Plague
/ Plague - immunology
/ Plague - microbiology
/ Plague - prevention & control
/ Plasmids
/ Polymorphism, Single Nucleotide - genetics
/ Pore Forming Cytotoxic Proteins - metabolism
/ Proteins
/ Receptors, Formyl Peptide - antagonists & inhibitors
/ Receptors, Formyl Peptide - deficiency
/ Receptors, Formyl Peptide - genetics
/ Receptors, Formyl Peptide - metabolism
/ Science
/ Science (multidisciplinary)
/ Translocation
/ Type III Secretion Systems - drug effects
/ U937 Cells
/ Vaccines
/ Yersinia pestis
/ Yersinia pestis - chemistry
/ Yersinia pestis - immunology
/ Yersinia pestis - metabolism
/ Yersinia pestis - pathogenicity
2019
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FPR1 is the plague receptor on host immune cells
by
Charlton, Thomas M.
, Osei-Owusu, Patrick
, Schneewind, Olaf
, Missiakas, Dominique
, Kim, Hwan Keun
in
13/106
/ 13/109
/ 13/31
/ 13/51
/ 14/19
/ 14/63
/ 631/250/255/1318
/ 631/326/421
/ 64/60
/ 82/29
/ 82/83
/ Alleles
/ Analysis
/ Animals
/ Antibodies
/ Antigens, Bacterial - metabolism
/ Bacteria
/ Bacterial Adhesion
/ Causes of
/ Cell receptors
/ Chemotaxis - immunology
/ CRISPR
/ CRISPR-Cas Systems
/ Destruction
/ Development and progression
/ Disease Models, Animal
/ Female
/ Gene expression
/ Genomes
/ HEK293 Cells
/ Human behavior
/ Humanities and Social Sciences
/ Humans
/ Immune response
/ Immune system
/ Infections
/ Infectious diseases
/ LcrV protein
/ Leukocytes (neutrophilic)
/ Macrophages - cytology
/ Macrophages - immunology
/ Macrophages - metabolism
/ Macrophages - microbiology
/ Male
/ Mice
/ Mice, Inbred C57BL
/ multidisciplinary
/ Mutation
/ Neoplasms
/ Neutrophils
/ Neutrophils - cytology
/ Neutrophils - immunology
/ Neutrophils - metabolism
/ Neutrophils - microbiology
/ Pandemics
/ Pathogens
/ Physiological aspects
/ Plague
/ Plague - immunology
/ Plague - microbiology
/ Plague - prevention & control
/ Plasmids
/ Polymorphism, Single Nucleotide - genetics
/ Pore Forming Cytotoxic Proteins - metabolism
/ Proteins
/ Receptors, Formyl Peptide - antagonists & inhibitors
/ Receptors, Formyl Peptide - deficiency
/ Receptors, Formyl Peptide - genetics
/ Receptors, Formyl Peptide - metabolism
/ Science
/ Science (multidisciplinary)
/ Translocation
/ Type III Secretion Systems - drug effects
/ U937 Cells
/ Vaccines
/ Yersinia pestis
/ Yersinia pestis - chemistry
/ Yersinia pestis - immunology
/ Yersinia pestis - metabolism
/ Yersinia pestis - pathogenicity
2019
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Journal Article
FPR1 is the plague receptor on host immune cells
2019
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Overview
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
R190W
as a candidate resistance allele in humans that protects neutrophils from destruction by the
Y. pestis
type III secretion system. Thus, FPR1 is a plague receptor on immune cells in both humans and mice, and its absence or mutation provides protection against
Y. pestis
. Furthermore, plague selection of
FPR1
alleles appears to have shaped human immune responses towards other infectious diseases and malignant neoplasms.
The receptor FPR1 on human immune cells interacts with
Yersinia pestis
, mutations in this receptor provide resistance against plague in humans and
Fpr1
deficiency enhances survival in mice.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 13/109
/ 13/31
/ 13/51
/ 14/19
/ 14/63
/ 64/60
/ 82/29
/ 82/83
/ Alleles
/ Analysis
/ Animals
/ Antigens, Bacterial - metabolism
/ Bacteria
/ CRISPR
/ Female
/ Genomes
/ Humanities and Social Sciences
/ Humans
/ Male
/ Mice
/ Mutation
/ Plague
/ Plague - prevention & control
/ Plasmids
/ Polymorphism, Single Nucleotide - genetics
/ Pore Forming Cytotoxic Proteins - metabolism
/ Proteins
/ Receptors, Formyl Peptide - antagonists & inhibitors
/ Receptors, Formyl Peptide - deficiency
/ Receptors, Formyl Peptide - genetics
/ Receptors, Formyl Peptide - metabolism
/ Science
/ Type III Secretion Systems - drug effects
/ Vaccines
/ Yersinia pestis - immunology
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