Evidence map›Paper›PMID 9108082›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1997

"Autoimmune rejection" of neonatal heart transplants in experimental Chagas disease is a parasite-specific response to infected host tissue.

R L Tarleton, L Zhang, M O Downs

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
9.6field-weighted citation impact, top 1% 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

47 citing papers in PubMed, 147 citations in OpenAlex.

  1. Trial
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  5. New insights intoFrontiers in immunology · 2024
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  19. VNI cures acute and chronic experimental Chagas disease.The Journal of infectious diseases · 2013
    Article
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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

3 authors at 1 institution in 1 country.

R L TarletonDepartment of Cellular Biology, The University of Georgia, Athens 30602, USA.
L Zhang
M O Downs
University of Georgia · US

Funding

IMMUNOREGULATION IN EXPERIMENTAL CHAGAS'DISEASER01AI022070 · NIAID · UNIVERSITY OF GEORGIA (UGA) · PI TARLETON, RICK L · 1985 to 2011
$3.2M
CD8+ T-CELLS AND TRYPANOSOMA CRUZI INFECTIONSR01AI033106 · NIAID · UNIVERSITY OF GEORGIA (UGA) · PI TARLETON, RICK L · 1994 to 2009
$2.8M
NIAID NIH HHS AI-22070NIAID NIH HHS AI-33106NIAID NIH HHS R01 AI022070NIAID NIH HHS R01 AI033106
6 · The paper itself

Abstract

Infection with the protozoan parasite Trypanosoma cruzi often results in chronic heart- and gut-associated disease known as Chagas disease. In this study we show that contrary to previous reports, neonatal hearts transplanted into mice chronically infected with T. cruzi do not exhibit signs of autoimmune-type rejection or any significant inflammatory response. In addition to an absence of inflammation, these syngeneic heart transplants survive for more than 1 year and are absolutely free of parasites as determined by in situ PCR analysis. However, if well-established transplanted hearts in chronically infected mice are directly injected with live parasites, a rapid and dramatic inflammatory response ensues that results in cessation of heart function. Likewise, transplanted hearts established in mice prior to systemic infection with T. cruzi or hearts transplanted into mice during the acute stage of T. cruzi infection become parasitized and develop inflammatory foci. In these cases where the transplanted hearts become parasitized, the ensuing inflammatory response is nearly identical to that observed in the native hearts of T. cruzi-infected mice in terms of cell types present and adhesion molecules and cytokines expressed. Importantly, this response is strikingly different from that observed in the allogeneic heart rejection. These results clearly document that parasitization of heart tissue is both necessary and sufficient for the induction of tissue damage in Chagas disease and strongly argue against a principal autoimmune etiology for this disease.

Indexed as

AnimalsAntibodies, ProtozoanAntigens, ProtozoanAutoimmunityChagas DiseaseFemaleGraft RejectionHeart TransplantationMiceMice, Inbred C3HMice, Inbred C57BLTrypanosoma cruziAntibodies, ProtozoanAntigens, Protozoan

Identifiers

PMID9108082
PMCPMC20545
OpenAlexW2039191904

What OpenQuestion holds

Textmetadata
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.