Evidence map›Paper›PMID 9094996›Full record

ArticleThe American journal of pathology1997

Differential pathogenesis of lethal mousepox in congenic DBA/2 mice implicates natural killer cell receptor NKR-P1 in necrotizing hepatitis and the fifth component of complement in recruitment of circulating leukocytes to spleen.

D G Brownstein, L Gras

Abstract readComparative Study
In one paragraph

Article in The American journal of pathology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

15 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Poxvirus tropism.Nature reviews. Microbiology · 2005
    Review
  8. Natural killer cell immune responses.Immunologic research · 2005
    Review
  9. Review
  10. Recognition of a virus-encoded ligand by a natural killer cell activation receptor.Proceedings of the National Academy of Sciences of the United States of America · 2002
    Article
  11. Article
  12. Enhanced resistance in STAT6-deficient mice to infection with ectromelia virus.Proceedings of the National Academy of Sciences of the United States of America · 2001
    Article
  13. Article
  14. Article
  15. Review
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

2 authors at 1 institution in 1 country.

D G BrownsteinSection of Comparative Medicine, Yale University School of Medicine, New Haven, CT 06520-8016, USA.
L Gras
Yale University · US

Funding

RESPONSES OF INBRED MICE TO ECTROMELIA VIRUSR01RR002053 · NCRR · YALE UNIVERSITY · PI BROWNSTEIN, DAVID G · 1992 to 1997
–
NCRR NIH HHS R01-RR02053
6 · The paper itself

Abstract

Innate resistance of C57BL/6 (B6) mice to lethal mousepox is controlled by multiple genes. Previously, four resistance genes were localized to specific subchromosomal regions and transferred onto a susceptible DBA/2 (D2) background by serial backcrossing and intercrossing to produce congenic strains. Intraperitoneally inoculated ectromelia virus was uniformly lethal and achieved similar titers in B6 and D2 mice but elicited differential responses in liver, spleen, and circulating blood leukocytes. The distribution of these response phenotypes in congenic strains linked control of phenotypes with specific subchromosomal regions. D2.R1 mice, which carried a differential segment of chromosome 6, exhibited a B6 liver response and intermediate spleen and circulating leukocyte responses. D2.R2 and D2.R4 mice, which carried differential segments of chromosomes 2 and 1, respectively, exhibited a D2 liver response, a B6 spleen response, and an intermediate circulating leukocyte response. The localization of control of liver response phenotypes to chromosome 6 implicates cells that express natural killer (NK) cell receptor NKR-P1 alloantigens. The localization of control of spleen and circulating leukocyte responses to chromosomes 1, 2, and 6 implicates NK cells, the fifth component of complement, and a gene near the selectin gene complex in recruitment of circulating leukocytes to spleen.

Indexed as

Lectins, C-TypeAnimalsAntigens, SurfaceChemotaxis, LeukocyteChromosome MappingComplement C5Crosses, GeneticEctromelia, InfectiousFemaleGenetic LinkageHepatitis, AnimalImmunity, InnateKiller Cells, NaturalLeukocyte CountMaleMiceAntigens, SurfaceComplement C5Lectins, C-TypeNK Cell Lectin-Like Receptor Subfamily B

Identifiers

PMID9094996
PMCPMC1858154
OpenAlexW282543996

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.