Evidence map›Paper›PMID 20656923›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2010

Regulation of virus-specific CD4+ T cell function by multiple costimulatory receptors during chronic HIV infection.

Afework Kassu, Roland A Marcus, Michelle B D'Souza, Elizabeth A Kelly-McKnight, Lucy Golden-Mason, Ramesh Akkina, Andrew P Fontenot, Cara C Wilson, Brent E Palmer

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 2 pooled it
3.3field-weighted citation impact, top 7% 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

73 citing papers in PubMed, 2 syntheses or guidelines pooled it, 108 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  6. Article
  7. Article
  8. The role of CD4MedComm · 2023
    Review
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  10. Article
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  16. Review
  17. CMIP is a negative regulator of T cell signaling.Cellular & molecular immunology · 2020
    Article
  18. Review
  19. Review
  20. Review

13 more citing papers are in PubMed but not listed here.

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

9 authors at 2 institutions in 1 country.

Afework KassuDivision of Allergy and Clinical Immunology, Department of Medicine, University of Colorado Denver, Aurora, CO 80045, USA.
Roland A Marcus
Michelle B D'Souza
Elizabeth A Kelly-McKnight
Lucy Golden-Mason
Ramesh Akkina
Andrew P Fontenot
Cara C Wilson
Brent E Palmer
University of Colorado Denver · USColorado State University · US

Funding

Patient-Oriented Research in Immunologic Lung Disease.K24HL102245 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI FONTENOT, ANDREW P. · 2010 to 2020
$1.4M
Enhancement of HIV-specific CD4+ T cell function by blockade of the PD-1 pathwayR21AI076161 · NIAID · UNIVERSITY OF COLORADO DENVER · PI PALMER, BRENT E · 2008 to 2009
$663k
NHLBI NIH HHS K24 HL102245NIAID NIH HHS 1R21 AI076161-01A2NIAID NIH HHS R21 AI076161
6 · The paper itself

Abstract

Elevated expression of inhibitory receptors on virus-specific T cells has been implicated as a mechanism by which viruses evade host immune surveillance. Blockade of these pathways during chronic infection leads to increased T cell function and improved immune control of viral replication. To explore the association between costimulatory receptors and HIV replication, we examined the expression of programmed death 1 (PD-1), CTLA-4, T cell Ig domain and mucin domain 3 (TIM-3), and CD28 on HIV-specific CD4(+) T cells from HIV-infected subjects. Greater than 30% of HIV-specific CD4(+) T cells from untreated subjects coexpressed PD-1, CTLA-4, and TIM-3, whereas <2% of CMV- or varicella-zoster virus-specific CD4(+) T cells expressed all three receptors. Coexpression of all three inhibitory receptors on HIV-specific CD4(+) T cells was more strongly correlated with viral load compared with the expression of each receptor individually. Suppression of HIV replication with antiretroviral therapy was associated with decreased expression of all three inhibitory receptors on HIV-specific CD4(+) T cells. Surprisingly, a high percentage of HIV-specific CD4(+) T cells that expressed inhibitory receptors also coexpressed CD28. In vitro blockade of PD-1 binding concurrent with stimulation through CD28 synergistically increased HIV-specific CD4(+) T cell proliferation to a greater extent than did either alone. These findings indicate that HIV-specific CD4(+) T cell responses during chronic infection are regulated by complex patterns of coexpressed inhibitory receptors and that the synergistic effect of inhibitory receptor blockade and stimulation of costimulatory receptors could be used for therapeutic augmentation of HIV-specific CD4(+) T cell function.

Indexed as

AdultCD4-Positive T-LymphocytesChronic DiseaseCohort StudiesEpitopes, T-LymphocyteHIV-1HIV InfectionsHumansReceptors, Antigen, T-CellEpitopes, T-LymphocyteReceptors, Antigen, T-Cell

Identifiers

PMID20656923
PMCPMC3985382
OpenAlexW2139496066

What OpenQuestion holds

Textmetadata
LicenceTDM
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.