ArticleThe Journal of biological chemistry2010
Trypanosoma cruzi subverts host cell sialylation and may compromise antigen-specific CD8+ T cell responses.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 58 citations in OpenAlex.
- Next-Generation Vaccines Against Neglected Diseases: New Promises from Genetically Modified Live-Attenuated Parasites and RNA Vaccines.Microorganisms · 2026Review
- Glycomics in Human Diseases and Its Emerging Role in Biomarker Discovery.Biomedicines · 2025Review
- Coinfection by multipleMicrobiology and molecular biology reviews : MMBR · 2025Review
- RNA and protein immunization withFrontiers in cellular and infection microbiology · 2025Article
- ST8Sia2 polysialyltransferase protects against infection by Trypanosoma cruzi.PLoS neglected tropical diseases · 2024Article
- Article
- Use ofFrontiers in microbiology · 2022Article
- Review
- Parasite-host glycan interactions during Trypanosoma cruzi infection: trans-Sialidase rides the show.Biochimica et biophysica acta. Molecular basis of disease · 2020Review
- Extracellular Vesicles in Trypanosomatids: Host Cell Communication.Frontiers in cellular and infection microbiology · 2020Review
- Overview of the role of kinetoplastid surface carbohydrates in infection and host cell invasion: prospects for therapeutic intervention.Parasitology · 2019Review
- CD43 sialoglycoprotein modulates cardiac inflammation and murine susceptibility to Trypanosoma cruzi infection.Scientific reports · 2019Article
- Metabolic Labeling of Surface Neo-sialylglyconjugates Catalyzed by Trypanosoma cruzi trans-Sialidase.Methods in molecular biology (Clifton, N.J.) · 2019Article
- Theft and Reception of Host Cell's Sialic Acid: Dynamics ofFrontiers in immunology · 2019Review
- Modulation of Immune Tolerance via Siglec-Sialic Acid Interactions.Frontiers in immunology · 2018Review
- Specific activation of CD4Clinical and experimental immunology · 2017Article
- βScientific reports · 2017Article
- The Trypanosoma cruzi Surface, a Nanoscale Patchwork Quilt.Trends in parasitology · 2017Review
- Role of Inactive and ActiveFrontiers in microbiology · 2017Article
- Long-Term Immunity to Trypanosoma cruzi in the Absence of Immunodominant trans-Sialidase-Specific CD8+ T Cells.Infection and immunity · 2016Article
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Upon activation, cytotoxic CD8(+) T lymphocytes are desialylated exposing beta-galactose residues in a physiological change that enhances their effector activity and that can be monitored on the basis of increased binding of the lectin peanut agglutinin. Herein, we investigated the impact of sialylation mediated by trans-sialidase, a specific and unique Trypanosoma transglycosylase for sialic acid, on CD8(+) T cell response of mice infected with T. cruzi. Our data demonstrate that T. cruzi uses its trans-sialidase enzyme to resialylate the CD8(+) T cell surface, thereby dampening antigen-specific CD8(+) T cell response that might favor its own persistence in the mammalian host. Binding of the monoclonal antibody S7, which recognizes sialic acid-containing epitopes on the 115-kDa isoform of CD43, was augmented on CD8(+) T cells from ST3Gal-I-deficient infected mice, indicating that CD43 is one sialic acid acceptor for trans-sialidase activity on the CD8(+) T cell surface. The cytotoxic activity of antigen-experienced CD8(+) T cells against the immunodominant trans-sialidase synthetic peptide IYNVGQVSI was decreased following active trans-sialidase-mediated resialylation in vitro and in vivo. Inhibition of the parasite's native trans-sialidase activity during infection strongly decreased CD8(+) T cell sialylation, reverting it to the glycosylation status expected in the absence of parasite manipulation increasing mouse survival. Taken together, these results demonstrate, for the first time, that T. cruzi subverts sialylation to attenuate CD8(+) T cell interactions with peptide-major histocompatibility complex class I complexes. CD8(+) T cell resialylation may represent a sophisticated strategy to ensure lifetime host parasitism.
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