ArticleInfection and immunity2015
Toll-like receptor 9 signaling in dendritic cells regulates neutrophil recruitment to inflammatory foci following Leishmania infantum infection.
Article in Infection and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 40 citations in OpenAlex.
- Article
- Neutrophil-based delivery platforms: from natural mechanisms to engineered therapeutics.Theranostics · 2026Review
- New insights into the life cycle, host cell tropism, and infection amplification ofInfection and immunity · 2025Review
- Toll-like Receptor-9 (TLR-9) Signaling Is Crucial for Inducing Protective Immunity following Immunization with Genetically Modified Live AttenuatedPathogens (Basel, Switzerland) · 2023Article
- Review
- Gene Signatures of Symptomatic and Asymptomatic Clinical-Immunological Profiles of Human Infection byMicroorganisms · 2023Article
- Paradoxical immune response in leishmaniasis: The role of toll-like receptors in disease progression.Parasite immunology · 2022Review
- Blood Bacteria-Free DNA in Septic Mice Enhances LPS-Induced Inflammation in Mice through Macrophage Response.International journal of molecular sciences · 2022Article
- Neutrophil Migratory Patterns: Implications for Cardiovascular Disease.Frontiers in cell and developmental biology · 2022Review
- PRMT5 inhibition modulates murine dendritic cells activation by inhibiting the metabolism switch: a new therapeutic target in periodontitis.Annals of translational medicine · 2021Article
- Microphysiological Systems for Studying Cellular Crosstalk During the Neutrophil Response to Infection.Frontiers in immunology · 2021Review
- The Impact of Neutrophil Recruitment to the Skin on the Pathology Induced byFrontiers in immunology · 2021Review
- Determinants of Innate Immunity in Visceral Leishmaniasis and Their Implication in Vaccine Development.Frontiers in immunology · 2021Review
- The Effects of Polyhexamethylene Biguanide (PHMB) and TLR Agonists Alone or as Polyplex Nanoparticles againstVeterinary sciences · 2020Article
- TLR4 abrogates the Th1 immune response through IRF1 and IFN-β to prevent immunopathology during L. infantum infection.PLoS pathogens · 2020Article
- TLR2 Signaling in Skin Nonhematopoietic Cells Induces Early Neutrophil Recruitment in Response to Leishmania major Infection.The Journal of investigative dermatology · 2019Article
- The role of TLR9 on Leishmania amazonensis infection and its influence on intranasal LaAg vaccine efficacy.PLoS neglected tropical diseases · 2019Article
- Molecular Aspects of Dendritic Cell Activation in Leishmaniasis: An Immunobiological View.Frontiers in immunology · 2019Review
- Genome-wide methylation analysis reveals differentially methylated loci that are associated with an age-dependent increase in bovine fibroblast response to LPS.BMC genomics · 2017Article
- Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Leishmania infantum is a protozoan parasite that causes visceral leishmaniasis (VL). This infection triggers dendritic cell (DC) activation through the recognition of microbial products by Toll-like receptors (TLRs). Among the TLRs, TLR9 is required for DC activation by different Leishmania species. We demonstrated that TLR9 is upregulated in vitro and in vivo during infection. We show that C57BL/6 mice deficient in TLR9 expression (TLR9(-/-) mice) are more susceptible to infection and display higher parasite numbers in the spleen and liver. The increased susceptibility of TLR9(-/-) mice was due to the impaired recruitment of neutrophils to the infection foci associated with reduced levels of neutrophil chemoattractants released by DCs in the target organs. Moreover, both Th1 and Th17 cells were also committed in TLR9(-/-) mice. TLR9-dependent neutrophil recruitment is mediated via the MyD88 signaling pathway but is TIR domain-containing adapter-inducing interferon beta (TRIF) independent. Furthermore, L. infantum failed to activate both plasmacytoid and myeloid DCs from TLR9(-/-) mice, which presented reduced surface costimulatory molecule expression and chemokine release. Interestingly, neutrophil chemotaxis was affected both in vitro and in vivo when DCs were derived from TLR9(-/-) mice. Our results suggest that TLR9 plays a critical role in neutrophil recruitment during the protective response against L. infantum infection that could be associated with DC activation.
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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.