Evidence map›Paper›PMID 12133998›Full record

ArticleJournal of virology2002

Novel role of CD8(+) T cells and major histocompatibility complex class I genes in the generation of protective CD4(+) Th1 responses during retrovirus infection in mice.

Karin E Peterson, Ingunn Stromnes, Ron Messer, Kim Hasenkrug, Bruce Chesebro

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

8 citing papers in PubMed, 20 citations in OpenAlex.

  1. Immunodominant CD4+ responses identified in a patient vaccinated with full-length NY-ESO-1 formulated with ISCOMATRIX adjuvant.Proceedings of the National Academy of Sciences of the United States of America · 2004
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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

5 authors at 2 institutions in 1 country.

Karin E PetersonLaboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana 59840, USA.
Ingunn Stromnes
Ron Messer
Kim Hasenkrug
Bruce Chesebro
National Institutes of Health · USNational Institute of Allergy and Infectious Diseases · US

Funding

Immunology And Pathology Of Acute Murine Leukemia Virus InfectionsZIAAI000753 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI HASENKRUG, KIM · 2009 to 2022
$8.1M
Immunology/Pathology Of Murine Leukemia Virus InfectionsZ01AI000753 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI HASENKRUG, KIM · 1996 to 2008
$3.5M
Pathogenesis/Immunology Of Animal And Human RetrovirusesZ01AI000074 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI CHESEBRO, BRUCE · 1985 to 2008
$445k
Pathogenesis And Immunology Of Animal And Human RetrovirusesZIAAI000074 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI CHESEBRO, BRUCE · 2009 to 2009
$46k
6 · The paper itself

Abstract

CD4(+) Th1 responses to virus infections are often necessary for the development and maintenance of virus-specific CD8(+) T-cell responses. However, in the present study with Friend murine retrovirus (FV), the reverse was also found to be true. In the absence of a responder H-2(b) allele at major histocompatibility complex (MHC) class II loci, a single H-2D(b) MHC class I allele was sufficient for the development of a CD4(+) Th1 response to FV. This effect of H-2D(b) on CD4(+) T-cell responses was dependent on CD8(+) T cells, as demonstrated by depletion studies. A direct effect of CD8(+) T-cell help in the development of CD4(+) Th1 responses to FV was also shown in vaccine studies. Vaccination of nonresponder H-2(a/a) mice induced FV-specific responses of H-2D(d)-restricted CD8(+) cytotoxic T lymphocytes (CTL). Adoptive transfer of vaccine-primed CD8(+) T cells to naive H-2(a/a) mice prior to infection resulted in the generation of FV-specific CD4(+) Th1 responses. This novel helper effect of CD8(+) T cells could be an important mechanism in the development of CD4(+) Th1 responses following vaccinations that induce CD8(+) CTL responses. The ability of MHC class I genes to facilitate CD4(+) Th1 development could also be considerable evolutionary advantage by allowing a wider variety of MHC genotypes to generate protective immune responses against intracellular pathogens.

Indexed as

Genes, MHC Class IAllelesAnimalsCD8-Positive T-LymphocytesCytokinesFriend murine leukemia virusGenes, MHC Class IIH-2 AntigensInterferon-gammaIn Vitro TechniquesLeukemia, ExperimentalLymphocyte ActivationMiceMice, CongenicMice, Inbred AMice, Inbred C57BLCytokinesH-2 AntigensInterferon-gamma

Identifiers

PMID12133998
PMCPMC155146
OpenAlexW2124181277

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.