Evidence map›Paper›PMID 25784743›Full record

ArticleJournal of leukocyte biology2015

Interferon-α inhibits CD4 T cell responses to interleukin-7 and interleukin-2 and selectively interferes with Akt signaling.

Thao P Nguyen, Doug A Bazdar, Joseph C Mudd, Michael M Lederman, Clifford V Harding, Gareth A Hardy, Scott F Sieg

Open access · greenAbstract read
In one paragraph

Article in Journal of leukocyte biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

14 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
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  12. Article
  13. Role of immune activation in progression to AIDS.Current opinion in HIV and AIDS · 2016
    Review
  14. CD8 T-Cell Expansion and Inflammation Linked to CMV Coinfection in ART-treated HIV Infection.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2016
    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

7 authors at 2 institutions in 1 country.

Thao P NguyenDepartments of *Medicine, Division of Infectious Diseases and HIV Medicine, and Pathology, Center for AIDS Research, Case Western Reserve University/University Hospitals Case Medical Center, Case Western Reserve University, Cleveland, Ohio, USA.
Doug A BazdarDepartments of *Medicine, Division of Infectious Diseases and HIV Medicine, and Pathology, Center for AIDS Research, Case Western Reserve University/University Hospitals Case Medical Center, Case Western Reserve University, Cleveland, Ohio, USA.
Joseph C MuddDepartments of *Medicine, Division of Infectious Diseases and HIV Medicine, and Pathology, Center for AIDS Research, Case Western Reserve University/University Hospitals Case Medical Center, Case Western Reserve University, Cleveland, Ohio, USA.
Michael M LedermanDepartments of *Medicine, Division of Infectious Diseases and HIV Medicine, and Pathology, Center for AIDS Research, Case Western Reserve University/University Hospitals Case Medical Center, Case Western Reserve University, Cleveland, Ohio, USA.
Clifford V HardingDepartments of *Medicine, Division of Infectious Diseases and HIV Medicine, and Pathology, Center for AIDS Research, Case Western Reserve University/University Hospitals Case Medical Center, Case Western Reserve University, Cleveland, Ohio, USA.
Gareth A HardyDepartments of *Medicine, Division of Infectious Diseases and HIV Medicine, and Pathology, Center for AIDS Research, Case Western Reserve University/University Hospitals Case Medical Center, Case Western Reserve University, Cleveland, Ohio, USA.
Scott F SiegDepartments of *Medicine, Division of Infectious Diseases and HIV Medicine, and Pathology, Center for AIDS Research, Case Western Reserve University/University Hospitals Case Medical Center, Case Western Reserve University, Cleveland, Ohio, USA sfs2@case.edu.
Case Western Reserve University · USUniversity Hospitals Case Medical Center · US

Funding

WG3: HIV, Co-infections and Co-morbiditiesP30AI036219 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI Sharon L. Hillier, JONATHAN KARN · 1994 to 2026
$50.0M
Regulation of macrophages by Mycobacterium tuberculosisR01AI034343 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI HARDING, CLIFFORD V · 1994 to 2017
$6.2M
Immunology Training Program-PredoctoralT32AI089474 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI COBB, BRIAN A · 2010 to 2025
$3.4M
Basic and Clinical Studies of CpG ODN in HIV DiseaseP01AI055793 · NIAID · RUSH UNIVERSITY MEDICAL CENTER · PI LANDAY, ALAN L · 2003 to 2004
$2.2M
M. tuberculosis lipoprotein-TLR2 interactionsR01AI069085 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI HARDING, CLIFFORD V · 2007 to 2011
$1.9M
Type I interferon as a mediator of immune failure in HIV diseaseR21AI104480 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI SIEG, SCOTT FREDERICK · 2013 to 2014
$424k
NIAID NIH HHS AI-036219NIAID NIH HHS AI-104480NIAID NIH HHS P01 AI055793NIAID NIH HHS P30 AI036219NIAID NIH HHS R01 AI034343NIAID NIH HHS R01 AI069085NIAID NIH HHS R21 AI104480NIAID NIH HHS T32 AI089474
6 · The paper itself

Abstract

Persistent type I IFN production occurs during chronic viral infections, such as HIV disease. As type I IFNs have antiproliferative activity, it is possible that chronic exposure to these cytokines could adversely affect T cell homeostasis. We investigated the capacity of IFN-α to impair T cell proliferation induced by the homeostatic cytokine, IL-7, or another common γ-chain cytokine, IL-2, in cells from healthy human donors. We found that IL-7- or IL-2-induced proliferation of CD4(+) T cells was partially inhibited in the presence of IFN-α. The CD4(+) T cells that were exposed to IFN-α also displayed attenuated induction of IL-2 and CD40L following TCR stimulation. Analyses of signaling pathways indicated that IL-7 and IL-2 induced a delayed and sustained P-Akt signal that lasted for several days and was partially inhibited by IFN-α. In contrast, IL-7-induced P-STAT5 was not affected by IFN-α. Furthermore, IFN-α had no detectable effect on P-Akt that was induced by the chemokine SDF-1. Both inhibitors of P-Akt and P-STAT5 blocked IL-7-induced T cell proliferation, confirming that both signaling pathways are important for IL-7-induced T cell proliferation. These results demonstrate that IFN-α can selectively inhibit cytokine-induced P-Akt as a potential mechanism to disrupt homeostasis of T lymphocytes.

Indexed as

CD40 LigandCD4 AntigensCD4-Positive T-LymphocytesCell ProliferationGene Expression RegulationHumansInterferon-alphaInterleukin-2Interleukin-7PhosphorylationPrimary Cell CultureProto-Oncogene Proteins c-aktReceptors, Antigen, T-CellSignal TransductionSTAT5 Transcription FactorCD40 LigandCD4 AntigensIL7 protein, humanInterferon-alphaInterleukin-2Interleukin-7Proto-Oncogene Proteins c-aktReceptors, Antigen, T-CellSTAT5 Transcription Factorcytokineshomeostatic proliferation

Identifiers

PMID25784743
PMCPMC4438745
OpenAlexW2107857955

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.