ArticleThe American journal of tropical medicine and hygiene2015
Deficiency in mannose-binding lectin-associated serine protease-2 does not increase susceptibility to Trypanosoma cruzi infection.
Article in The American journal of tropical medicine and hygiene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- The grand escape - how pathogens outsmart the human complement system.Immunobiology · 2025Review
- Immunothrombotic dysregulation in chagas disease and COVID-19: a comparative study of anticoagulation.Molecular and cellular biochemistry · 2021Article
- Is It Possible to Intervene in the Capacity ofFrontiers in immunology · 2021Review
- Complement Evasion: An Effective Strategy That Parasites Utilize to Survive in the Host.Frontiers in microbiology · 2019Review
- The Unsolved Jigsaw Puzzle of the Immune Response in Chagas Disease.Frontiers in immunology · 2018Review
- Review
- Escaping Deleterious Immune Response in Their Hosts: Lessons from Trypanosomatids.Frontiers in immunology · 2016Review
- MBL-associated serine proteases (MASPs) and infectious diseases.Molecular immunology · 2015Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
Trypanosoma cruzi is the causative agent of Chagas' disease, a chronic illness affecting 10 million people around the world. The complement system plays an important role in fighting microbial infections. The recognition molecules of the lectin pathway of complement activation, mannose-binding lectin (MBL), ficolins, and CL-11, bind to specific carbohydrates on pathogens, triggering complement activation through MBL-associated serine protease-2 (MASP-2). Previous in vitro work showed that human MBL and ficolins contribute to T. cruzi lysis. However, MBL-deficient mice are only moderately compromised in their defense against the parasite, as they may still activate the lectin pathway through ficolins and CL-11. Here, we assessed MASP-2-deficient mice, the only presently available mouse line with total lectin pathway deficiency, for a phenotype in T. cruzi infection. Total absence of lectin pathway functional activity did not confer higher susceptibility to T. cruzi infection, suggesting that it plays a minor role in the immune response against this parasite.
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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.