Evidence map›Paper›PMID 9348311›Full record

ArticleThe Journal of experimental medicine1997

Interferon (IFN) consensus sequence-binding protein, a transcription factor of the IFN regulatory factor family, regulates immune responses in vivo through control of interleukin 12 expression.

N A Giese, L Gabriele, T M Doherty, D M Klinman, L Tadesse-Heath, C Contursi, S L Epstein, H C Morse

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

59 citing papers in PubMed, 161 citations in OpenAlex.

  1. International journal of biological sciences · 2026
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  8. Transcription Factors Interplay Orchestrates the Immune-Metabolic Response ofFrontiers in cellular and infection microbiology · 2021
    Review
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  17. Relevance of Interferon Regulatory Factor-8 Expression in Myeloid-Tumor Interactions.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2016
    Review
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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

8 authors at 4 institutions in 1 country.

N A GieseLaboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892-0760, USA. ngiese@atlas.niaid.nih.gov
L Gabriele
T M Doherty
D M Klinman
L Tadesse-Heath
C Contursi
S L Epstein
H C Morse
National Institutes of Health · USEunice Kennedy Shriver National Institute of Child Health and Human Development · USCenter for Biologics Evaluation and Research · USNational Institute of Allergy and Infectious Diseases · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mice with a null mutation of the gene encoding interferon consensus sequence-binding protein (ICSBP) develop a chronic myelogenous leukemia-like syndrome and mount impaired responses to certain viral and bacterial infections. To gain a mechanistic understanding of the contributions of ICSBP to humoral and cellular immunity, we characterized the responses of control and ICSBP-/- mice to infection with influenza A (flu) and Leishmania major (L. major). Mice of both genotypes survived infections with flu, but differed markedly in the isotype distribution of antiflu antibodies. In sera of normal mice, immunoglobulin (Ig)G2a antibodies were dominant over IgG1 antibodies, a pattern indicative of a T helper cell type 1 (Th1)-driven response. In sera of ICSBP-/- mice, however, IgG1 antibodies dominated over IgG2a antibodies, a pattern indicative of a Th2-driven response. The dominance of IgG1 and IgE over IgG2a was detected in the sera of uninfected mice as well. A seeming Th2 bias of ICSBP-deficient mice was also uncovered in their inability to control infection with L. major, where resistance is known to be dependent on IL-12 and IFN-gamma as components of a Th1 response. Infected ICSBP-deficient mice developed fulminant, disseminated leishmaniasis as a result of failure to mount a Th1-mediated curative response, although T cells remained capable of secreting IFN-gamma and macrophages of producing nitric oxide. Compromised Th1 differentiation in ICSBP-/- mice could not be attributed to hyporesponsiveness of CD4(+) T cells to interleukin (IL)-12; however, the ability of uninfected and infected ICSBP-deficient mice to produce IL-12 was markedly impaired. This indicates that ICSBP is a deciding factor in Th responses governing humoral and cellular immunity through its role in regulating IL-12 expression.

Indexed as

Repressor ProteinsAnimalsCarrier ProteinsCell DifferentiationConsensus SequenceDisease SusceptibilityInfluenza A virusInterferon Regulatory Factor-8Interferon Regulatory FactorsInterferonsInterleukin-12Leishmania majorLeishmaniasis, CutaneousMiceMice, Inbred C57BLMice, KnockoutCarrier ProteinsInterferon Regulatory Factor-8Interferon Regulatory FactorsInterferonsInterleukin-12Repressor ProteinsTranscription Factors

Identifiers

PMID9348311
PMCPMC2199114
OpenAlexW2006786538

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.