Evidence map›Paper›PMID 7657839›Full record

ArticleThe Journal of clinical investigation1995

Priming for high interferon-gamma production induced by interleukin-12 in both CD4+ and CD8+ T cell clones from HIV-infected patients.

C Paganin, I Frank, G Trinchieri

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of clinical investigation, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

13 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Interleukin-12 in infectious diseases.Clinical microbiology reviews · 1997
    Review
  10. Article
  11. Article
  12. Immune dysregulation and CD4+ T cell loss in HIV-1 infection.Springer seminars in immunopathology · 1997
    Review
  13. Article
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 2 institutions in 1 country.

C PaganinWistar Institute of Anatomy and Biology, Philadelphia, Pennsylvania 19104, USA.
I Frank
G Trinchieri
Hospital of the University of Pennsylvania · USThe Wistar Institute · US

Funding

Tumor Microenvironment and MetastasisP30CA010815 · NCI · WISTAR INSTITUTE · PI Maureen E. Murphy · 1985 to 2026
$75.9M
CELL-MEDIATED CYTOTOXICITY IN HUMANSR01CA020833 · NCI · WISTAR INSTITUTE · PI KAUFMAN, RUSSEL E. · 1985 to 2003
$1.9M
DIFFERENTIATION AND FUNCTION OF MONOCYTESR01CA032898 · NCI · WISTAR INSTITUTE · PI SANTOLI, DANIELA · 1985 to 1994
–
CELL-MEDIATED CYTOTOXICITY IN HUMANSR37CA020833 · NCI · WISTAR INSTITUTE · PI TRINCHIERI, GIORGIO · 1990 to 1998
–
NCI NIH HHS CA 10815NCI NIH HHS CA 20833NCI NIH HHS CA32898
6 · The paper itself

Abstract

HIV-infected patients are defective in their ability to produce interleukin (IL)-12 in vitro in response to pathogenic bacteria and parasites. IL-12 enhances the patient's depressed natural killer cell cytotoxic activity, peripheral blood lymphocyte production of interferon-gamma (IFN-gamma), and proliferative T cell response in vitro to recall antigens, HIV antigens, alloantigens, and mitogens. However, these effects represent short-lived responses and imply the need for chronic IL-12 therapeutic administration in the clinical setting. To identify any long-term effects of IL-12 on T cell differentiation toward Th1 cells, peripheral blood T cells from 10 HIV-infected patients at different stages of disease were cloned by limiting dilution in the presence or absence of IL-12 and tested for cytokine production in response to stimulation with anti-CD3 antibodies and phorbol diesters IL-12 present during the first 2 wk of clonal expansion determined a stable severalfold enhancement on the ability of both CD4+ and CD8+ clones to produce IFN-gamma. Because priming for high IFN-gamma production is probably the most important mechanism by which IL-12 induces generation of efficient T helper type 1 (Th1) cells, these results suggest the possibility that IL-12 treatment in vivo of HIV-infected patients may stimulate a protective Th1 response against opportunistic pathogens and possibly HIV itself.

Indexed as

AntibodiesAntibodies, MonoclonalCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesClone CellsHIV InfectionsHumansImmunophenotypingInterferon-gammaInterleukin-12Interleukin-4Lymphocyte ActivationPhytohemagglutininsRecombinant ProteinsReference ValuesTetradecanoylphorbol AcetateAntibodiesAntibodies, MonoclonalInterferon-gammaInterleukin-12Interleukin-4PhytohemagglutininsRecombinant ProteinsTetradecanoylphorbol Acetate

Identifiers

PMID7657839
PMCPMC185796
OpenAlexW2021451157

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.