ArticlePLoS pathogens2010
Impaired innate immunity in Tlr4(-/-) mice but preserved CD8+ T cell responses against Trypanosoma cruzi in Tlr4-, Tlr2-, Tlr9- or Myd88-deficient mice.
Article in PLoS pathogens, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 79 citations in OpenAlex.
- Immunization with the Tc85-Derived Peptide Displayed on Virus-like Particles Confers Protection againstACS omega · 2026Article
- Cardiac alterations induced by Trypanosoma cruzi extracellular vesicles and immune complexes.PLoS neglected tropical diseases · 2025Article
- Towards a map of the immune system manipulation network byFrontiers in cellular and infection microbiology · 2025Review
- cGAS-STING Pathway Activation during Trypanosoma cruzi Infection Leads to Tissue-Dependent Parasite Control.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- From Benznidazole to New Drugs: Nanotechnology Contribution in Chagas Disease.International journal of molecular sciences · 2023Review
- Genetic Ablation and Pharmacological Blockade of Bradykinin B1 Receptor Unveiled a Detrimental Role for the Kinin System in Chagas Disease Cardiomyopathy.Journal of clinical medicine · 2023Article
- Cytotoxic CD4eLife · 2022Article
- Statins change the cytokine profile inFrontiers in immunology · 2022Article
- Host-parasite dynamics in Chagas disease from systemic to hyper-local scales.Parasite immunology · 2021Review
- STING Signaling Drives Production of Innate Cytokines, Generation of CD8Frontiers in immunology · 2021Article
- Virulence ofFrontiers in cellular and infection microbiology · 2021Article
- Effect of theParasitology · 2020Article
- São Paulo School of Advanced Sciences on Vaccines: an overview.The journal of venomous animals and toxins including tropical diseases · 2020Review
- Understanding CD8Trends in parasitology · 2019Review
- CD43 sialoglycoprotein modulates cardiac inflammation and murine susceptibility to Trypanosoma cruzi infection.Scientific reports · 2019Article
- In-silico design of a multi-epitope vaccine candidate against onchocerciasis and related filarial diseases.Scientific reports · 2019Article
- MyD88 activation in cardiomyocytes contributes to the heart immune response to acute Trypanosoma cruzi infection with no effect on local parasite control.PLoS neglected tropical diseases · 2018Article
- Pathogenesis of Chronic Chagas Disease: Macrophages, Mitochondria, and Oxidative Stress.Current clinical microbiology reports · 2018Article
- Disease Tolerance and Pathogen Resistance Genes May UnderlieFrontiers in immunology · 2018Article
- Article
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Authors and funding
13 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The murine model of T. cruzi infection has provided compelling evidence that development of host resistance against intracellular protozoans critically depends on the activation of members of the Toll-like receptor (TLR) family via the MyD88 adaptor molecule. However, the possibility that TLR/MyD88 signaling pathways also control the induction of immunoprotective CD8+ T cell-mediated effector functions has not been investigated to date. We addressed this question by measuring the frequencies of IFN-gamma secreting CD8+ T cells specific for H-2K(b)-restricted immunodominant peptides as well as the in vivo Ag-specific cytotoxic response in infected animals that are deficient either in TLR2, TLR4, TLR9 or MyD88 signaling pathways. Strikingly, we found that T. cruzi-infected Tlr2(-/-), Tlr4(-/-), Tlr9(-/) (-) or Myd88(-/-) mice generated both specific cytotoxic responses and IFN-gamma secreting CD8+ T cells at levels comparable to WT mice, although the frequency of IFN-gamma+CD4+ cells was diminished in infected Myd88(-/-) mice. We also analyzed the efficiency of TLR4-driven immune responses against T. cruzi using TLR4-deficient mice on the C57BL genetic background (B6 and B10). Our studies demonstrated that TLR4 signaling is required for optimal production of IFN-gamma, TNF-alpha and nitric oxide (NO) in the spleen of infected animals and, as a consequence, Tlr4(-/-) mice display higher parasitemia levels. Collectively, our results indicate that TLR4, as well as previously shown for TLR2, TLR9 and MyD88, contributes to the innate immune response and, consequently, resistance in the acute phase of infection, although each of these pathways is not individually essential for the generation of class I-restricted responses against T. cruzi.
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