ArticleInfection and immunity2015
Trypanosoma cruzi trans-sialidase prevents elicitation of Th1 cell response via interleukin 10 and downregulates Th1 effector cells.
Article in Infection and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 31 citations in OpenAlex.
- Review
- Chagas disease: host responses, parasite evasion and vaccine advances.Transactions of the Royal Society of Tropical Medicine and Hygiene · 2026Review
- Sex in Immune Cells and Parasitic Diseases - A Complex Relationship.Immunological reviews · 2026Review
- Variation in surface protein expression leads to heterogeneous Trypanosoma cruzi populations during host cell infection.Nature communications · 2025Article
- Galectin-8 deficiency promotes chronic splenomegaly persistence in Chagas disease.Frontiers in cellular and infection microbiology · 2025Article
- RNA and protein immunization withFrontiers in cellular and infection microbiology · 2025Article
- Intranasal Trans-Sialidase Vaccine Mitigates Acute and Chronic Pathology in a Preclinical Oral Chagas Disease Model.Vaccines · 2024Article
- Sialic acid removal by trans-sialidase modulates MMP-2 activity during Trypanosoma cruzi infection.Biochimie · 2021Article
- Sialic Acids as Receptors for Pathogens.Biomolecules · 2021Review
- Host-parasite dynamics in Chagas disease from systemic to hyper-local scales.Parasite immunology · 2021Review
- Review
- Article
- Parasite-host glycan interactions during Trypanosoma cruzi infection: trans-Sialidase rides the show.Biochimica et biophysica acta. Molecular basis of disease · 2020Review
- Pathology and Pathogenesis of Chagas Heart Disease.Annual review of pathology · 2019Review
- Theft and Reception of Host Cell's Sialic Acid: Dynamics ofFrontiers in immunology · 2019Review
- The Unsolved Jigsaw Puzzle of the Immune Response in Chagas Disease.Frontiers in immunology · 2018Review
- Purinergic Antagonist Suramin Aggravates Myocarditis and Increases Mortality by Enhancing Parasitism, Inflammation, and Reactive Tissue Damage inOxidative medicine and cellular longevity · 2018Article
- Trans-sialidase-based vaccine candidate protects againstOncotarget · 2017Article
- The Trypanosoma cruzi Surface, a Nanoscale Patchwork Quilt.Trends in parasitology · 2017Review
- Role of Inactive and ActiveFrontiers in microbiology · 2017Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
The trans-sialidases (TSs) from Trypanosoma cruzi, the agent of Chagas disease, are virulence factors shed to the bloodstream that induce strong alterations in the immune system. Here, we report that both enzymatically active TS (aTS) and its lectinlike isoform (iTS) disturb CD4 T cell physiology, inducing downregulation of Th1 cell functionality and in vivo cell expansion. By using ovalbumin-specific DO11.10 cells as tracers of clones developing the Th1 phenotype, we found that the infection induced significant amounts of gamma interferon (IFN-γ) but low levels of interleukin 2 (IL-2) and increased IL-4 production in vivo, in agreement with a mixed T helper response. The production of cytokines associated with the Th2 phenotype was prevented by passive transfer of anti-TS neutralizing antibodies. TSs also reduced the T cell receptor signaling as assayed by Zap-70 phosphorylation. TSs also reduced IL-2 and IFN-γ secretion, with a concomitant increase in IL-4 production and then an unbalancing of the CD4 T cell response toward the Th2 phenotype. This effect was prevented by using anti-IL-10 neutralizing antibodies or IL-10(-/-) antigen-presenting cells, supporting the subversion of this regulatory pathway. In support, TSs stimulated IL-10 secretion by antigen-presenting cells during their interaction with CD4 T cells. When polarized cells were stimulated in the presence of TSs, the secretion of IL-2 and IFN-γ was strongly downregulated in Th1 cells, while IL-2 production was upregulated in Th2 cells. Although the Th1 response is associated with host survival, it may simultaneously induce extensive damage to infected tissues. Thus, by delaying the elicitation of the Th1 response and limiting its effector properties, TSs restrain the cell response, supporting T. cruzi colonization and persistence while favoring host survival.
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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.