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Cited by 67Trypanosoma species research and implicationsResearch on Leishmaniasis StudiesGlycosylation and Glycoproteins Research

Immune Evasion Strategies of Trypanosoma cruzi

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Flávia Nardy, Ana, Freire-de-Lima, Célio Geraldo, Morrot, Alexandre·2015·Journal of Immunology Research
DOI 10.1155/2015/178947PMC PMC4512591
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Abstract

Microbes have evolved a diverse range of strategies to subvert the host immune system. The protozoan parasite Trypanosoma cruzi , the causative agent of Chagas disease, provides a good example of such adaptations. This parasite targets a broad spectrum of host tissues including both peripheral and central lymphoid tissues. Rapid colonization of the host gives rise to a systemic acute response which the parasite must overcome. The parasite in fact undermines both innate and adaptive immunity. It interferes with the antigen presenting function of dendritic cells via an action on host sialic acid-binding Ig-like lectin receptors. These receptors also induce suppression of CD4 + T cells responses, and we presented evidence that the sialylation of parasite-derived mucins is required for the inhibitory effects on CD4 T cells. In this review we highlight the major mechanisms used by Trypanosoma cruzi to overcome host immunity and discuss the role of parasite colonization of the central thymic lymphoid tissue in chronic disease.

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  • As a result, immature T-lymphocytes are released from the thymic central tolerance and differentiate into mature T-helper cells in the lymph nodes.

    “As a result, immature T-lymphocytes are released from the thymic central tolerance and differentiate into mature T-helper cells in the lymph nodes (Flávia Nardy et al., 2015).”

    From Identification of Candidate Signature Genes and Key Regulators Associated With Trypanotolerance in the Sheko Breed (2019) · cites this paper as Flávia Nardy et al., 2015

    Section 3 (page not provided) reports premature release of immature thymocytes from the infected thymus into the periphery. It does not say they differentiate into mature T-helper cells in lymph nodes; it also reports that the infected thymus retains the ability to carry out negative selection, rather than establishing that these cells escape central tolerance. (LLM, conf=0.86)

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Authors
Flávia Nardy, A., Freire-de-Lima, C. G., & Morrot, A.
Affiliations
  • Instituto de Microbiologia, Universidade Federal do Rio de Janeiro, 21.941-590 Rio de Janeiro, RJ, Brazil
  • Universidade Federal do Rio de Janeiro (BR)
Corresponding author
  • Freire-de-Lima, Célio Geraldo
  • Morrot, Alexandre
ORCID
Venue
Journal of Immunology Research
Publisher
Wiley
Published
2015
Volume
2015
Pages
1-7
ISSN
  • 2314-7156 (ISSN-L)
  • 2314-8861
DOI
10.1155/2015/178947
PMC
PMC4512591
OpenAlex
W1516061070
Cited by
67
References
0
Citations by year
2026: 5 · 2025: 5 · 2024: 6 · 2023: 3 · 2022: 8 · 2021: 5 · 2020: 3 · 2019: 8 · 2018: 7 · 2017: 6 · 2016: 8 · 2015: 3
FWCI
1.04
Type
journal article
Language
en
Open access
Licence
Locations
  • Journal of Immunology Research (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
Funders
  • Fundação de Amparo à Pesquisa do Estado do Rio de Janeiro
  • Conselho Nacional de Desenvolvimento Científico e Tecnológico
Topics
  • Health Sciences › Medicine › Epidemiology › Trypanosoma species research and implications
  • Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Research on Leishmaniasis Studies
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Glycosylation and Glycoproteins Research
Keywords
Trypanosoma cruzi, Chagas disease, immune evasion, dendritic cells, antigen presentation, CD4+ T cell suppression, thymus colonization, chronic infection, innate immunity, adaptive immunity
MeSH terms
Host-Parasite Interactions, Humans, Immune Tolerance, Trypanosoma cruzi, Chagas Disease, T-Lymphocyte Subsets, Virulence Factors, Immune Evasion, Disease Resistance

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