ArticleClinical and vaccine immunology : CVI2009
Yersinia pestis can bypass protective antibodies to LcrV and activation with gamma interferon to survive and induce apoptosis in murine macrophages.
Article in Clinical and vaccine immunology : CVI, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Live attenuated vaccines alone or in combination with an adenovirus-based vaccine protect mice lacking IFN-γ against pneumonic plague.Science translational medicine · 2026Article
- Functional assays to screen and select monoclonal antibodies that targetHuman vaccines & immunotherapeutics · 2023Article
- Antibody Opsonization Enhances Early Interactions between Yersinia pestis and Neutrophils in the Skin and Draining Lymph Node in a Mouse Model of Bubonic Plague.Infection and immunity · 2020Article
- Guanylate Binding Proteins Regulate Inflammasome Activation in Response to Hyperinjected Yersinia Translocon Components.Infection and immunity · 2017Article
- Macrophage cell death upon intracellular bacterial infection.Macrophage · 2015Article
- Article
- Random mutagenesis identifies a C-terminal region of YopD important for Yersinia type III secretion function.PloS one · 2015Article
- Direct neutralization of type III effector translocation by the variable region of a monoclonal antibody to Yersinia pestis LcrV.Clinical and vaccine immunology : CVI · 2014Article
- Intranasal prophylaxis with CpG oligodeoxynucleotide can protect against Yersinia pestis infection.Infection and immunity · 2013Article
- Surface organelles assembled by secretion systems of Gram-negative bacteria: diversity in structure and function.FEMS microbiology reviews · 2012Review
- Opposing roles for interferon regulatory factor-3 (IRF-3) and type I interferon signaling during plague.PLoS pathogens · 2012Article
- Insight into bacterial virulence mechanisms against host immune response via the Yersinia pestis-human protein-protein interaction network.Infection and immunity · 2011Article
- Chemokine receptor CXCR2 mediates bacterial clearance rather than neutrophil recruitment in a murine model of pneumonic plague.The American journal of pathology · 2011Article
- Host Defense and the Airway Epithelium: Frontline Responses That Protect against Bacterial Invasion and Pneumonia.Journal of pathogens · 2011Article
- A Yersinia effector protein promotes virulence by preventing inflammasome recognition of the type III secretion system.Cell host & microbe · 2010Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Yersinia pestis, the agent of plague, uses a type III secretion injectisome to deliver Yop proteins into macrophages to counteract phagocytosis and induce apoptosis. Additionally, internalized Y. pestis can survive in the phagosomes of naïve or gamma interferon (IFN-gamma)-activated macrophages by blocking vacuole acidification. The Y. pestis LcrV protein is a target of protective antibodies. The binding of antibodies to LcrV at the injectisome tip results in neutralization of the apoptosis of Y. pestis-infected macrophages and is used as an in vitro correlate of protective immunity. The cytokines IFN-gamma and tumor necrosis factor alpha can cooperate with anti-LcrV to promote protection against lethal Y. pestis infection in mice. It is not known if these phagocyte-activating cytokines cooperate with anti-LcrV to increase the killing of the pathogen and decrease apoptosis in macrophages. We investigated how anti-LcrV and IFN-gamma impact bacterial survival and apoptosis in cultured murine macrophages infected with Y. pestis KIM5. Y. pestis KIM5 opsonized with polyclonal or monoclonal anti-LcrV was used to infect macrophages treated with or without IFN-gamma. The phagocytosis and survival of KIM5 and the apoptosis of macrophages were measured at different time points postinfection. The results show that anti-LcrV reduced apoptosis at an early time point (5 h) but not at a later time point (24 h). Polyclonal anti-LcrV was unable to inhibit apoptosis at either time point in IFN-gamma-activated macrophages. Additionally, anti-LcrV was ineffective at promoting the killing of KIM5 in naïve or activated macrophages. We conclude that Y. pestis can bypass protective antibodies to LcrV and activation with IFN-gamma to survive and induce apoptosis in murine macrophages.
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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.