ArticlePLoS pathogens2011
The Trypanosoma cruzi protease cruzain mediates immune evasion.
Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 120 citations in OpenAlex.
- Review
- Caco-2 Cell Co-Culture Alters the Molecular Size of Igl1 and Its Extracellular Fragments inPathogens (Basel, Switzerland) · 2026Article
- Cruzain Inhibitors for Chagas Disease: Anticorrelated Optimisation Landscapes and the Multiparametric Path to Clinical Candidates.Chemical biology & drug design · 2026Review
- To Explore Potential Natural Inhibitors of Cysteine Proteases to Combat Human African Trypanosomiasis and Chagas Disease.Current medicinal chemistry · 2026Review
- Sex in Immune Cells and Parasitic Diseases - A Complex Relationship.Immunological reviews · 2026Review
- Comparative 5' IsomiRome Analysis Uncovers Dysregulated 5' IsomiRs inComputational and structural biotechnology journal · 2026Article
- Unraveling Common Patterns and Differences among Cruzipains through Molecular Dynamics Simulations and Structural Analyses.ACS omega · 2025Article
- Cystatin from Austrelaps superbus snake venom as a model for identifying potential inhibitors of Trypanosoma cruzi cruzain.The journal of venomous animals and toxins including tropical diseases · 2025Article
- Investigation of the activity of 4-aminoquinolines as cysteine protease inhibitors with application in the treatment of Chagas disease.Memorias do Instituto Oswaldo Cruz · 2025Article
- Towards a map of the immune system manipulation network byFrontiers in cellular and infection microbiology · 2025Review
- Drug Discovery Efforts to Identify Novel Treatments for Neglected Tropical Diseases - Cysteine Protease Inhibitors.Current medicinal chemistry · 2024Review
- Oral infectivity through carnivorism in murine model ofFrontiers in cellular and infection microbiology · 2024Article
- From Benznidazole to New Drugs: Nanotechnology Contribution in Chagas Disease.International journal of molecular sciences · 2023Review
- Covalent Inhibitors for Neglected Diseases: An Exploration of Novel Therapeutic Options.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Article
- Immunopathological Mechanisms Underlying Cardiac Damage in Chagas Disease.Pathogens (Basel, Switzerland) · 2023Review
- Screening the Pathogen Box to Discover and Characterize New Cruzain andPathogens (Basel, Switzerland) · 2023Article
- First Molecular Identification of Trypanosomes and Absence ofPathogens (Basel, Switzerland) · 2022Article
- The Role of Nuclear Factor Kappa B (NF-κB) in the Immune Response against Parasites.Pathogens (Basel, Switzerland) · 2022Review
- Synthesis and biological evaluation in vitro and in silico of N-propionyl-N'-benzeneacylhydrazone derivatives as cruzain inhibitors of Trypanosoma cruzi.Molecular diversity · 2022Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Trypanosoma cruzi is the causative agent of Chagas' disease. Novel chemotherapy with the drug K11777 targets the major cysteine protease cruzain and disrupts amastigote intracellular development. Nevertheless, the biological role of the protease in infection and pathogenesis remains unclear as cruzain gene knockout failed due to genetic redundancy. A role for the T. cruzi cysteine protease cruzain in immune evasion was elucidated in a comparative study of parental wild type- and cruzain-deficient parasites. Wild type T. cruzi did not activate host macrophages during early infection (<60 min) and no increase in ∼P iκB was detected. The signaling factor NF-κB P65 colocalized with cruzain on the cell surface of intracellular wild type parasites, and was proteolytically cleaved. No significant IL-12 expression occurred in macrophages infected with wild type T. cruzi and treated with LPS and BFA, confirming impairment of macrophage activation pathways. In contrast, cruzain-deficient parasites induced macrophage activation, detectable iκB phosphorylation, and nuclear NF-κB P65 localization. These parasites were unable to develop intracellularly and survive within macrophages. IL 12 expression levels in macrophages infected with cruzain-deficient T. cruzi were comparable to LPS activated controls. Thus cruzain hinders macrophage activation during the early (<60 min) stages of infection, by interruption of the NF-κB P65 mediated signaling pathway. These early events allow T. cruzi survival and replication, and may lead to the spread of infection in acute Chagas' disease.
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