ArticleInfection and immunity2013
Toll-like receptor 6 plays an important role in host innate resistance to Brucella abortus infection in mice.
Article in Infection and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 49 citations in OpenAlex.
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- Toll-like receptor 6 inhibits colorectal cancer progression by suppressing NF-κB signaling.Heliyon · 2024Article
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- Varying conjunctival immune response adaptations of house finch populations to a rapidly evolving bacterial pathogen.Frontiers in immunology · 2024Article
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- Toll-like Receptor Mediation in SARS-CoV-2: A Therapeutic Approach.International journal of molecular sciences · 2022Review
- Galectin-3 regulates proinflammatory cytokine function and favours Brucella abortus chronic replication in macrophages and mice.Cellular microbiology · 2021Article
- MyD88-Dependent Glucose Restriction and Itaconate Production Control Brucella Infection.Infection and immunity · 2021Article
- Toll-Like Receptors: Expression and Roles in Otitis Media.International journal of molecular sciences · 2021Review
- Whole-Genome Resequencing to Study Brucellosis Susceptibility in Sheep.Frontiers in genetics · 2021Article
- ASC-Mediated Inflammation and Pyroptosis AttenuatesPathogens (Basel, Switzerland) · 2020Article
- Dendritic cells and Brucella spp. interaction: the sentinel host and the stealthy pathogen.Folia microbiologica · 2020Review
- Immunopathogenesis of Hepatic Brucellosis.Frontiers in cellular and infection microbiology · 2019Review
- Immunoproteasome Subunits Are Required for CD8Infection and immunity · 2018Article
- Comparative RNA-sequencing analysis of ER-based HSP90 functions and signal pathways in Tribolium castaneum.Cell stress & chaperones · 2018Article
- Temporal Role for MyD88 in a Model of Brucella-Induced Arthritis and Musculoskeletal Inflammation.Infection and immunity · 2017Article
- The Calcium-Induced Regulation in the Molecular and Transcriptional Circuitry of Human Inflammatory Response and Autoimmunity.Frontiers in pharmacology · 2017Article
- TLR7 and TLR3 SenseFrontiers in immunology · 2017Article
- Functional Impairment of Murine Dendritic Cell Subsets following Infection with Infective Larval Stage 3 of Brugia malayi.Infection and immunity · 2017Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brucella abortus is recognized by several Toll-like receptor (TLR)-associated pathways triggering proinflammatory responses that affect both the nature and intensity of the immune response. Previously, we demonstrated that B. abortus-mediated dendritic cell (DC) maturation and control of infection are dependent on the adaptor molecule MyD88. However, the involvement of all TLRs in response to B. abortus infection is not completely understood. Therefore, we decided to evaluate the requirement for TLR6 in host resistance to B. abortus. Here, we demonstrated that TLR6 is an important component for triggering an innate immune response against B. abortus. An in vitro luciferase assay indicated that TLR6 cooperates with TLR2 to sense Brucella and further activates NF-κB signaling. However, in vivo analysis showed that TLR6, not TLR2, is required for the efficient control of B. abortus infection. Additionally, B. abortus-infected dendritic cells require TLR6 to induce tumor necrosis factor alpha (TNF-α) and interleukin-12 (IL-12). Furthermore, our findings demonstrated that the mitogen-activated protein kinase (MAPK) signaling pathway is impaired in TLR2, TLR6, and TLR2/6 knockout (KO) DCs when infected with B. abortus, which may account for the lower proinflammatory cytokine production observed in TLR6 KO mouse dendritic cells. In summary, the results presented here indicate that TLR6 is required to trigger innate immune responses against B. abortus in vivo and is required for the full activation of DCs to induce robust proinflammatory cytokine production.
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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.