Evidence map›Paper›PMID 36695605›Full record

ArticlemSphere2023

Delayed Activation of T Cells at the Site of Infection Facilitates the Establishment of Trypanosoma cruzi in Both Naive and Immune Hosts.

Angel M Padilla, Charles Rosenberg, Peter Cook, Fernando Sanchez-Valdez, Caroline McElhannon, Rick L Tarleton

Open access · goldAbstract read
In one paragraph

Article in mSphere, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.6field-weighted citation impact, top 6% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 17 citations in OpenAlex.

  1. Vaccines against chronicExpert review of vaccines · 2026
    Review
  2. Glycosomal Phosphoenolpyruvate Carboxykinase CRISPR/Cas9-Deletion and Its Role in Trypanosoma cruzi Metacyclogenesis and Infectivity in Mammalian Host.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Chagas disease in immunocompromised patients.Clinical microbiology reviews · 2024
    Review
  12. Article
  13. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 2 countries.

Angel M PadillaDepartment of Cellular Biology, University of Georgia, Athens, Georgia, USA.ORCID 0000-0002-7907-5667
Charles RosenbergCenter for Tropical and Emerging Global Diseases, University of Georgia, Athens, Georgia, USA.
Peter CookMedical Research Council Centre for Medical Mycology, University of Exeter, Exeter, United Kingdom.
Fernando Sanchez-ValdezCenter for Tropical and Emerging Global Diseases, University of Georgia, Athens, Georgia, USA.
Caroline McElhannonDepartment of Cellular Biology, University of Georgia, Athens, Georgia, USA.
Rick L TarletonDepartment of Cellular Biology, University of Georgia, Athens, Georgia, USA.
University of Georgia · USUniversity of Exeter · GB

Funding

Trypanosoma cruzi dormancy and its implications for therapeutic treatmentR01AI151148 · NIAID · UNIVERSITY OF GEORGIA · PI TARLETON, RICK L · 2020 to 2024
$2.4M
Mechanisms of persistence in Trypanosoma cruzi infectionR01AI124692 · NIAID · UNIVERSITY OF GEORGIA · PI TARLETON, RICK L · 2016 to 2020
$1.9M
Medical Research Council MR/V033417/1NIAID NIH HHS R01 AI124692NIAID NIH HHS R01 AI151148
6 · The paper itself

Abstract

Although parasite entry through breaks in the skin or mucosa is one of the main routes of natural transmission of Trypanosoma cruzi, little is known about the host cell types initially invaded nor the ability of those host cells to initiate immune responses at the site of infection. To gain insights into these early events, we studied the fate of fluorescently tagged T. cruzi delivered subcutaneously in mouse footpads or ears. We demonstrate that the majority of parasites introduced into the skin initially proliferate there until 8 to 10 days postinfection, when the parasite load decreases. This decline in parasite numbers is dependent on the presence of an intact T cell compartment and on the ability of hosts to produce gamma interferon (IFN-γ). Many of the parasite-containing cells at the initial infection site display a macrophage/monocyte phenotype but with low expression of activation markers, suggesting that these cells provide an early niche for T. cruzi proliferation, rather than being active in parasite control. It is only after the first round of T. cruzi replication and release from host cells that signs of immune activation and control of parasites become apparent. The delay in the activation and failure to rapidly control parasite replication are observed even when T. cruzi-primed T cells are present, such as in chronically infected mice. This failure of a primed immune system to recognize and react prior to extensive parasite expansion at the infection site likely poses a significant challenge for the development of vaccines aiming to prevent T. cruzi infection.

Indexed as

Chagas DiseaseTrypanosoma cruziAnimalsInterferon-gammaMacrophagesMiceT-LymphocytesInterferon-gammasite of infectionT cellsTrypanosoma cruzi

Identifiers

PMID36695605
PMCPMC9942555
OpenAlexW4317939794

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.