ArticleInfection and immunity2013
Role of Toll-like receptor 9 signaling in experimental Leishmania braziliensis infection.
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 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Accuracy of mucocutaneous leishmaniasis diagnosis using polymerase chain reaction: systematic literature review and meta-analysis.Memorias do Instituto Oswaldo Cruz · 2015Pooled it
- Photodynamic inactivation of Leishmania braziliensis doubly sensitized with uroporphyrin and diamino-phthalocyanine activates effector functions of macrophages in vitro.Scientific reports · 2020Article
- TLR9/MyD88/TRIF signaling activates host immune inhibitory CD200 in Leishmania infection.JCI insight · 2019Article
- The role of TLR9 on Leishmania amazonensis infection and its influence on intranasal LaAg vaccine efficacy.PLoS neglected tropical diseases · 2019Article
- Article
- Redundant and regulatory roles for Toll-like receptors in Leishmania infection.Clinical and experimental immunology · 2017Review
- Local Delivery of the Toll-Like Receptor 9 Ligand CpG Downregulates Host Immune and Inflammatory Responses, Ameliorating Established Leishmania (Viannia) panamensis Chronic Infection.Infection and immunity · 2017Article
- Infection of Human Monocytes withFrontiers in immunology · 2017Article
- Alternative to Chemotherapy-The Unmet Demand against Leishmaniasis.Frontiers in immunology · 2017Review
- Leishmania major Infection-Induced VEGF-A/VEGFR-2 Signaling Promotes Lymphangiogenesis That Controls Disease.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Cathepsin B-Deficient Mice Resolve Leishmania major Inflammation Faster in a T Cell-Dependent Manner.PLoS neglected tropical diseases · 2016Article
- Dendritic Cells and Leishmania Infection: Adding Layers of Complexity to a Complex Disease.Journal of immunology research · 2016Review
- Article
- Toll-like receptor 9 signaling in dendritic cells regulates neutrophil recruitment to inflammatory foci following Leishmania infantum infection.Infection and immunity · 2015Article
- Innate immunity against Leishmania infections.Cellular microbiology · 2015Review
- Leishmania infantum amastigotes trigger a subpopulation of human B cells with an immunoregulatory phenotype.PLoS neglected tropical diseases · 2015Article
- Enhanced expression of Toll-like receptors 2 and 4, but not 9, in spleen tissue from patients with visceral leishmaniasis.Parasite immunology · 2014Article
- TLR9 activation is triggered by the excess of stimulatory versus inhibitory motifs present in Trypanosomatidae DNA.PLoS neglected tropical diseases · 2014Article
- The immunological, environmental, and phylogenetic perpetrators of metastatic leishmaniasis.Trends in parasitology · 2014Review
- Repeated exposure to Lutzomyia intermedia sand fly saliva induces local expression of interferon-inducible genes both at the site of injection in mice and in human blood.PLoS neglected tropical diseases · 2014Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infection with Leishmania braziliensis causes cutaneous or mucocutaneous leishmaniasis in humans. Toll-like receptor 9 (TLR9) expression has been found in granulomas of lesions in L. braziliensis-infected individuals. L. braziliensis inoculation in mice induces very small lesions that are self-healing, whereas deficiency in the TLR adaptor molecule, MyD88, renders mice susceptible to infection. The TLR involved has not been identified, prompting us to investigate if TLR9 triggering by the parasite contributes to the strong resistance to infection observed in L. braziliensis-inoculated mice. The parasites activated wild-type (WT) dendritic cells (DCs) in vitro but not DCs derived from TLR9(-/-) mice. TLR9(-/-) mice inoculated with L. braziliensis exhibited a transient susceptibility characterized by increased lesion size and parasite burden compared to those of WT mice. Surprisingly, elevated levels of gamma interferon (IFN-γ) were measured at the site of infection and in draining lymph node T cells of TLR9(-/-) mice at the peak of susceptibility, suggesting that unlike observations in vitro, the parasite could induce DC activation leading to the development of Th1 cells in the absence of TLR9 expression. Taken together, these data show that TLR9 signaling is important for the early control of lesion development and parasite burden but is dispensable for the differentiation of Th1 cells secreting IFN-γ, and the high levels of this cytokine are not sufficient to control early parasite replication following L. braziliensis infection.
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