ArticlePLoS pathogens2008
Distinct TLR- and NLR-mediated transcriptional responses to an intracellular pathogen.
Article in PLoS pathogens, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers.
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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.
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Who cites it
126 citing papers in PubMed, 213 citations in OpenAlex.
- Review
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- For Better or Worse: Type I Interferon Responses in Bacterial Infection.Pathogens (Basel, Switzerland) · 2025Review
- The balance between antiviral and antibacterial responses duringbioRxiv : the preprint server for biology · 2024Article
- Transcriptomic Analysis of Mycobacterial Infected Macrophages Reveals a High MOI Specific Type I IFN Signaling.Infection and immunity · 2023Article
- A nod to the bond between NOD2 and mycobacteria.PLoS pathogens · 2023Review
- Pathogenicity of Type I Interferons inInternational journal of molecular sciences · 2023Review
- Multifaceted roles and regulation of nucleotide-binding oligomerization domain containing proteins.Frontiers in immunology · 2023Review
- Genomic and pathogenicity islands ofFrontiers in molecular biosciences · 2023Review
- Review
- Type I interferon decreases macrophage energy metabolism during mycobacterial infection.Cell reports · 2021Article
- NOD1 and NOD2 in inflammatory and infectious diseases.Immunological reviews · 2020Review
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- Pathogenic Biohacking: Induction, Modulation and Subversion of Host Transcriptional Responses byToxins · 2020Review
- Why is Listeria monocytogenes such a potent inducer of CD8+ T-cells?Cellular microbiology · 2020Review
- Innate and Adaptive Immune Responses duringMicrobiology spectrum · 2019Article
- Article
- Type I interferons in tuberculosis: Foe and occasionally friend.The Journal of experimental medicine · 2018Review
- A Comparison of Oral and Intravenous Mouse Models of Listeriosis.Pathogens (Basel, Switzerland) · 2018Review
- Article
66 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
How the innate immune system tailors specific responses to diverse microbial infections is not well understood. Cells use a limited number of host receptors and signaling pathways to both discriminate among extracellular and intracellular microbes, and also to generate responses commensurate to each threat. Here, we have addressed these questions by using DNA microarrays to monitor the macrophage transcriptional response to the intracellular bacterial pathogen Listeria monocytogenes. By utilizing combinations of host and bacterial mutants, we have defined the host transcriptional responses to vacuolar and cytosolic bacteria. These compartment-specific host responses induced significantly different sets of target genes, despite activating similar transcription factors. Vacuolar signaling was entirely MyD88-dependent, and induced the transcription of pro-inflammatory cytokines. The IRF3-dependent cytosolic response induced a distinct set of target genes, including IFNbeta. Many of these cytosolic response genes were induced by secreted cytokines, so we further identified those host genes induced independent of secondary signaling. The host response to cytosolic bacteria was reconstituted by the cytosolic delivery of L. monocytogenes genomic DNA, but we observed an amplification of this response by NOD2 signaling in response to MDP. Correspondingly, the induction of IFNbeta was reduced in nod2-/- macrophages during infection with either L. monocytogenes or Mycobacterium tuberculosis. Combinatorial control of IFNbeta induction by recognition of both DNA and MDP may highlight a mechanism by which the innate immune system integrates the responses to multiple ligands presented in the cytosol by intracellular pathogens.
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Registered trials
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.