ArticlePLoS pathogens2009
NFATc1 mediates Toll-like receptor-independent innate immune responses during Trypanosoma cruzi infection.
Article in PLoS pathogens, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 40 citations in OpenAlex.
- Integrative Genomics Identifies Candidate Genes Underlying Trypanotolerance in Hybrid African Cattle.Evolutionary applications · 2026Article
- Chagas disease: host responses, parasite evasion and vaccine advances.Transactions of the Royal Society of Tropical Medicine and Hygiene · 2026Review
- NFATc1 in CD4The journal of allergy and clinical immunology. Global · 2025Article
- Article
- Host-parasite dynamics in Chagas disease from systemic to hyper-local scales.Parasite immunology · 2021Review
- Drug-cured experimental Trypanosoma cruzi infections confer long-lasting and cross-strain protection.PLoS neglected tropical diseases · 2020Article
- Pathogenesis of Chronic Chagas Disease: Macrophages, Mitochondria, and Oxidative Stress.Current clinical microbiology reports · 2018Article
- Article
- Calcineurin-NFAT signalling in myeloid leucocytes: new prospects and pitfalls in immunosuppressive therapy.EMBO molecular medicine · 2017Review
- BATF2 inhibits immunopathological Th17 responses by suppressingThe Journal of experimental medicine · 2017Article
- The Wnt5a-Ror2 axis promotes the signaling circuit between interleukin-12 and interferon-γ in colitis.Scientific reports · 2015Article
- Acteoside inhibits type Ι allergy through the down-regulation of Ca/NFAT and JNK MAPK signaling pathways in basophilic cells.Journal of natural medicines · 2013Article
- Trypanosoma cruzi infection and endothelin-1 cooperatively activate pathogenic inflammatory pathways in cardiomyocytes.PLoS neglected tropical diseases · 2013Article
- CD3-T cell receptor co-stimulation through SLAMF3 and SLAMF6 receptors enhances RORγt recruitment to the IL17A promoter in human T lymphocytes.The Journal of biological chemistry · 2012Article
- Trypanosoma cruzi activates cord blood myeloid dendritic cells independently of cell infection.Medical microbiology and immunology · 2012Article
- The kallikrein-kinin system in experimental Chagas disease: a paradigm to investigate the impact of inflammatory edema on GPCR-mediated pathways of host cell invasion by Trypanosoma cruzi.Frontiers in immunology · 2012Article
- Nonimmune Cells Contribute to Crosstalk between Immune Cells and Inflammatory Mediators in the Innate Response to Trypanosoma cruzi Infection.Journal of parasitology research · 2012Article
- The Immune Response to Trypanosoma cruzi: Role of Toll-Like Receptors and Perspectives for Vaccine Development.Journal of parasitology research · 2012Article
- Invasion and intracellular survival by protozoan parasites.Immunological reviews · 2011Review
- Impaired innate immunity in Tlr4(-/-) mice but preserved CD8+ T cell responses against Trypanosoma cruzi in Tlr4-, Tlr2-, Tlr9- or Myd88-deficient mice.PLoS pathogens · 2010Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Host defense against the intracellular protozoan parasite Trypanosoma cruzi depends on Toll-like receptor (TLR)-dependent innate immune responses. Recent studies also suggest the presence of TLR-independent responses to several microorganisms, such as viruses, bacteria, and fungi. However, the TLR-independent responses to protozoa remain unclear. Here, we demonstrate a novel TLR-independent innate response pathway to T. cruzi. Myd88(-/-)Trif(-/-) mice lacking TLR signaling showed normal T. cruzi-induced Th1 responses and maturation of dendritic cells (DCs), despite high sensitivity to the infection. IFN-gamma was normally induced in T. cruzi-infected Myd88(-/-)Trif(-/-) innate immune cells, and further was responsible for the TLR-independent Th1 responses and DC maturation after T. cruzi infection. T. cruzi infection induced elevation of the intracellular Ca(2+) level. Furthermore, T. cruzi-induced IFN-gamma expression was blocked by inhibition of Ca(2+) signaling. NFATc1, which plays a pivotal role in Ca(2+) signaling in lymphocytes, was activated in T. cruzi-infected Myd88(-/-)Trif(-/-) innate immune cells. T. cruzi-infected Nfatc1(-/-) fetal liver DCs were impaired in IFN-gamma production and DC maturation. These results demonstrate that NFATc1 mediates TLR-independent innate immune responses in T. cruzi infection.
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