ArticleInfection and immunity2006
Virulent Salmonella enterica serovar typhimurium evades adaptive immunity by preventing dendritic cells from activating T cells.
Article in Infection and immunity, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed.
- A pan-genome perspective on the evolutionary dynamics of polyphyly, virulence, and antibiotic resistance inCurrent research in food science · 2025Article
- Dual RNA sequencing reveals dendritic cell reprogramming in response to typhoidal Salmonella invasion.Communications biology · 2022Article
- Differential responses of chicken monocyte-derived dendritic cells infected with Salmonella Gallinarum and Salmonella Typhimurium.Scientific reports · 2021Article
- How the PhoP/PhoQ System Controls Virulence and MgMicrobiology and molecular biology reviews : MMBR · 2021Review
- New Insights on the Early Interaction Between Typhoid and Non-typhoidFrontiers in microbiology · 2021Review
- The Tumour Suppressor TMEM127 Is a Nedd4-Family E3 Ligase Adaptor Required by Salmonella SteD to Ubiquitinate and Degrade MHC Class II Molecules.Cell host & microbe · 2020Article
- Review
- Review
- Bacteria That Cause Enteric Diseases Stimulate Distinct Humoral Immune Responses.Frontiers in immunology · 2020Review
- Article
- Controversy Surrounding the Function of SpiC Protein inFrontiers in microbiology · 2019Review
- Immune-Modulation by the Human Respiratory Syncytial Virus: Focus on Dendritic Cells.Frontiers in immunology · 2019Review
- PersistentFrontiers in immunology · 2018Article
- Guanylate Binding Proteins Regulate Inflammasome Activation in Response to Hyperinjected Yersinia Translocon Components.Infection and immunity · 2017Article
- The protection role of Atg16l1 in CD11cImmunobiology · 2017Article
- Interleukin-10 Production by T and B Cells Is a Key Factor to Promote SystemicFrontiers in immunology · 2017Article
- The Salmonella Effector SteD Mediates MARCH8-Dependent Ubiquitination of MHC II Molecules and Inhibits T Cell Activation.Cell host & microbe · 2016Article
- Live and inactivated Salmonella enterica serovar Typhimurium stimulate similar but distinct transcriptome profiles in bovine macrophages and dendritic cells.Veterinary research · 2016Article
- Direct visualization of endogenous Salmonella-specific B cells reveals a marked delay in clonal expansion and germinal center development.European journal of immunology · 2015Article
- Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dendritic cells (DCs) constitute the link between innate and adaptive immunity by directly recognizing pathogen-associated molecular patterns (PAMPs) in bacteria and by presenting bacterial antigens to T cells. Recognition of PAMPs renders DCs as professional antigen-presenting cells able to prime naïve T cells and initiate adaptive immunity against bacteria. Therefore, interfering with DC function would promote bacterial survival and dissemination. Understanding the molecular mechanisms that have evolved in virulent bacteria to evade activation of adaptive immunity requires the characterization of virulence factors that interfere with DC function. Salmonella enterica serovar Typhimurium, the causative agent of typhoid-like disease in the mouse, can prevent antigen presentation to T cells by avoiding lysosomal degradation in DCs. Here, we show that this feature of virulent Salmonella applies in vivo to prevent activation of adaptive immunity. In addition, this attribute of virulent Salmonella requires functional expression of a type three secretion system (TTSS) and effector proteins encoded within the Salmonella pathogenicity island 2 (SPI-2). In contrast to wild-type virulent Salmonella, mutant strains carrying specific deletions of SPI-2 genes encoding TTSS components or effectors proteins are targeted to lysosomes and are no longer able to prevent DCs from activating T cells in vitro or in vivo. SPI-2 mutant strains are attenuated in vivo, showing reduced tissue colonization and enhanced T-cell activation, which confers protection against a challenge with wild-type virulent Salmonella. Our data suggest that impairment of DC function by the activity of SPI-2 gene products is crucial for Salmonella pathogenesis.
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