Evidence map›Paper›PMID 10570179›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1999

Granzymes are the essential downstream effector molecules for the control of primary virus infections by cytolytic leukocytes.

A Müllbacher, P Waring, R Tha Hla, T Tran, S Chin, T Stehle, C Museteanu, M M Simon

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

67 citing papers in PubMed, 199 citations in OpenAlex.

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  4. The adenovirus DNA-binding protein DBP.Journal of virology · 2024
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7 more citing papers are in PubMed but not listed here.

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

8 authors at 2 institutions in 2 countries.

A MüllbacherDivision of Immunology, John Curtin School of Medical Research, Australian National University, Canberra ACT 2601, Australia. arno.mullbacher@anu.edu.au
P Waring
R Tha Hla
T Tran
S Chin
T Stehle
C Museteanu
M M Simon
Australian National University · AUMax Planck Institute of Immunobiology and Epigenetics · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Analysis of perforin-deficient mice has identified the cytolytic pathway and perforin as the preeminent effector molecule in T cell-mediated control of virus infections. In this paper, we show that mice lacking both granzyme A (gzmA) and granzyme B (gzmB), which are, beside perforin, key constituents of cytolytic vesicles, are as incapable as are perforin-deficient mice of controlling primary infections by the natural mouse pathogen ectromelia, a poxvirus. Death of gzmAxgzmB double knockout mice occurred in a dose-dependent manner, despite the expression of functionally active perforin and the absence of an intrinsic defect to generate splenic cytolytic T cells. These results establish that both gzmA and gzmB are indispensable effector molecules acting in concert with perforin in granule exocytosis-mediated host defense against natural viral pathogens.

Indexed as

AnimalsCell DeathCell LineChromium IsotopesCytotoxicity, ImmunologicEctromelia, InfectiousEctromelia virusFemaleGranzymesHumansLeukocytesLiverMaleMembrane GlycoproteinsMiceMice, Inbred C57BLChromium IsotopesGranzymesGZMA protein, humanGZMB protein, humanGzmb protein, mouseMembrane GlycoproteinsPerforinPore Forming Cytotoxic ProteinsSerine Endopeptidases

Identifiers

PMID10570179
PMCPMC24171
OpenAlexW2146329250

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.