ReviewWorld journal of experimental medicine2013
Modulation of immune response in experimental Chagas disease.
Review in World journal of experimental medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 62 citations in OpenAlex.
- Therapeutic potential of hookworm proteins in promoting regulatory immune responses to modulate Trypanosoma cruzi induced liver inflammation and oxidative stress.Memorias do Instituto Oswaldo Cruz · 2026Article
- Chagas Disease in the 21st Century: Global Spread, Ecological Shifts, and Research Frontiers.Biology · 2025Review
- Cardiac alterations induced by Trypanosoma cruzi extracellular vesicles and immune complexes.PLoS neglected tropical diseases · 2025Article
- Profile of soluble cell adhesion molecules as potential biomarkers in the cardiac stages of chronic Chagas disease.Frontiers in immunology · 2025Article
- Differential Regulation of L-Arginine Metabolism through NOS2 and Arginases during Infection withPathogens (Basel, Switzerland) · 2024Article
- The Functions of Cytokines in the Cardiac Immunopathogenesis of Chagas Disease.Pathogens (Basel, Switzerland) · 2024Review
- Immunization with a Trypanosoma cruzi cyclophilin-19 deletion mutant protects against acute Chagas disease in mice.NPJ vaccines · 2023Article
- Article
- Interleukin-32Journal of immunology research · 2022Article
- Combined use of real-time PCR and serological techniques for improved surveillance of chronic and acute American trypanosomiasis in dogs and their owners from an endemic rural area of Neotropical Mexico.Current research in parasitology & vector-borne diseases · 2022Article
- Administration of artinm lectin reduces the severity of the acute phase infection withFASEB bioAdvances · 2021Article
- Biomarkers and Their Possible Functions in the Intestinal Microenvironment of Chagasic Megacolon: An Overview of the (Neuro)inflammatory Process.Journal of immunology research · 2021Review
- The First Contact of Human Dendritic Cells WithFrontiers in immunology · 2021Article
- Immunomodulation for the Treatment of Chronic Chagas Disease Cardiomyopathy: A New Approach to an Old Enemy.Frontiers in cellular and infection microbiology · 2021Review
- Early Immune Response Elicited by DifferentFrontiers in cellular and infection microbiology · 2021Article
- Electrolyzed Oxidizing Water Modulates the Immune Response in BALB/c Mice Experimentally Infected withPathogens (Basel, Switzerland) · 2020Article
- MicroRNA-155 Deficiency Exacerbates Trypanosoma cruzi Infection.Infection and immunity · 2020Article
- Review
- Effects of ghrelin supplementation on the acute phase of Chagas disease in rats.Parasites & vectors · 2019Article
- Correlation of Parasite Burden, kDNA Integration, Autoreactive Antibodies, and Cytokine Pattern in the Pathophysiology of Chagas Disease.Frontiers in microbiology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Trypanosoma cruzi (T. cruzi), the etiological agent of Chagas disease, affects nearly 18 million people in Latin America and 90 million are at risk of infection. The parasite presents two stages of medical importance in the host, the amastigote, intracellular replicating form, and the extracellular trypomastigote, the infective form. Thus infection by T. cruzi induces a complex immune response that involves effectors and regulatory mechanisms. That is why control of the infection requires a strong humoral and cellular immune response; hence, the outcome of host-parasite interaction in the early stages of infection is extremely important. A critical event during this period of the infection is innate immune response, in which the macrophage's role is vital. Thus, after being phagocytized, the parasite is able to develop intracellularly; however, during later periods, these cells induce its elimination by means of toxic metabolites. In turn, as the infection progresses, adaptive immune response mechanisms are triggered through the TH1 and TH2 responses. Finally, T. cruzi, like other protozoa such as Leishmania and Toxoplasma, have numerous evasive mechanisms to the immune response that make it possible to spread around the host. In our Laboratory we have developed a vaccination model in mice with Trypanosoma rangeli, nonpathogenic to humans, which modulates the immune response to infection by T. cruzi, thus protecting them. Vaccinated animals showed an important innate response (modulation of NO and other metabolites, cytokines, activation of macrophages), a strong adaptive cellular response and significant increase in specific antibodies. The modulation caused early elimination of the parasites, low parasitaemia, the absence of histological lesions and high survival rates. Even though progress has been made in the knowledge of some of these mechanisms, new studies must be conducted which could target further prophylactic and therapeutic trials against T. cruzi infection.
Indexed as
Identifiers
What OpenQuestion holds
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.