ArticleInfection and immunity2000
Involvement of CD4(+) Th1 cells in systemic immunity protective against primary and secondary challenges with Trypanosoma cruzi.
Article in Infection and immunity, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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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.
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Who cites it
49 citing papers in PubMed, 102 citations in OpenAlex.
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- An Update on Vaccines AgainstPathogens (Basel, Switzerland) · 2025Review
- Different responses involving Tfh cells delay parasite-specific antibody production inFrontiers in immunology · 2025Article
- Animal models for exploring Chagas disease pathogenesis and supporting drug discovery.Clinical microbiology reviews · 2024Review
- Immunization with a Trypanosoma cruzi cyclophilin-19 deletion mutant protects against acute Chagas disease in mice.NPJ vaccines · 2023Article
- Exploring the performance of Escherichia coli outer membrane vesicles as a tool for vaccine development against Chagas disease.Memorias do Instituto Oswaldo Cruz · 2023Article
- Aplastic Anemia and Chagas Disease:Tropical medicine and infectious disease · 2022Article
- Incomplete Recruitment of Protective T Cells Is Associated with Trypanosoma cruzi Persistence in the Mouse Colon.Infection and immunity · 2022Article
- Use ofFrontiers in microbiology · 2022Article
- Emerging and reemerging forms of Trypanosoma cruzi transmission.Memorias do Instituto Oswaldo Cruz · 2022Review
- Th17 Cells Provide Mucosal Protection against Gastric Trypanosoma cruzi Infection.Infection and immunity · 2021Article
- 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
- The Blockade of Interleukin-2 During the Acute Phase ofFrontiers in cellular and infection microbiology · 2021Article
- Lessons Learned for Pathogenesis, Immunology, and Disease of Erythrocytic Parasites:Frontiers in cellular and infection microbiology · 2021Review
- Parasite-host glycan interactions during Trypanosoma cruzi infection: trans-Sialidase rides the show.Biochimica et biophysica acta. Molecular basis of disease · 2020Review
- A prophylactic α-Gal-based glycovaccine effectively protects against murine acute Chagas disease.NPJ vaccines · 2019Article
- Advances in nanocarriers as drug delivery systems in Chagas disease.International journal of nanomedicine · 2019Review
- Trypanosoma cruzi 80 kDa prolyl oligopeptidase (Tc80) as a novel immunogen for Chagas disease vaccine.PLoS neglected tropical diseases · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
In general, gamma interferon (IFN-gamma)-producing CD4(+) Th1 cells are important for the immunological control of intracellular pathogens. We previously demonstrated an association between parasite-specific induction of IFN-gamma responses and resistance to the intracellular protozoan Trypanosoma cruzi. To investigate a potential causal relationship between Th1 responses and T. cruzi resistance, we studied the ability of Th1 cells to protect susceptible BALB/c mice against virulent parasite challenges. We developed immunization protocols capable of inducing polarized Th1 and Th2 responses in vivo. Induction of parasite-specific Th1 responses, but not Th2 responses, protected BALB/c mice against virulent T. cruzi challenges. We generated T. cruzi-specific CD4(+) Th1 and Th2 cell lines from BALB/c mice that were activated by infected macrophages to produce their corresponding cytokine response profiles. Th1 cells, but not Th2 cells, induced nitric oxide production and inhibited intracellular parasite replication in T. cruzi-infected macrophages. Despite the ability to inhibit parasite replication in vitro, Th1 cells alone could not adoptively transfer protection against T. cruzi to SCID mice. In addition, despite the fact that the adoptive transfer of CD4(+) T lymphocytes was shown to be necessary for the development of immunity protective against primary T. cruzi infection in our SCID mouse model, protective secondary effector functions could be transferred to SCID mice from memory-immune BALB/c mice in the absence of CD4(+) T lymphocytes. These results indicate that, although CD4(+) Th1 cells can directly inhibit intracellular parasite replication, a more important role for these cells in T. cruzi systemic immunity may be to provide helper activity for the development of other effector functions protective in vivo.
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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.