Evidence map›Paper›PMID 23913962›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2013

Selective induction of CTL helper rather than killer activity by natural epitope variants promotes dendritic cell-mediated HIV-1 dissemination.

Robbie B Mailliard, Kellie N Smith, Ronald J Fecek, Giovanna Rappocciolo, Eduardo J M Nascimento, Ernesto T Marques, Simon C Watkins, James I Mullins, Charles R Rinaldo

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

29 citing papers in PubMed, 36 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Role of CXCR5Frontiers in microbiology · 2022
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Dendritic Cell-Based Cancer Vaccines.Journal of immunology (Baltimore, Md. : 1950) · 2018
    Review
  16. Review
  17. Linked in: immunologic membrane nanotube networks.Journal of leukocyte biology · 2016
    Review
  18. Article
  19. Article
  20. 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

9 authors at 2 institutions in 1 country.

Robbie B MailliardDepartment of Infectious Diseases and Microbiology, University of Pittsburgh, Pittsburgh, PA 15261, USA. rbm19@pitt.edu
Kellie N Smith
Ronald J Fecek
Giovanna Rappocciolo
Eduardo J M Nascimento
Ernesto T Marques
Simon C Watkins
James I Mullins
Charles R Rinaldo
University of Pittsburgh · USUniversity of Washington · US

Funding

University of Pittsburgh Multicenter AIDS Cohort Study (MACS)U01AI035041 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MARTINSON, JEREMY JAMES, RINALDO, CHARLES R · 1993 to 2018
$71.4M
Viral Determinants of HIV-1 Transmission in African HeterosexualsP01AI057005 · NIAID · UNIVERSITY OF WASHINGTON · PI COREY, LAWRENCE · 2003 to 2014
$20.5M
Anti-HIV T Cell Responses During Antiviral Drug TherapyR37AI041870 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI RINALDO, CHARLES R · 2004 to 2013
$3.3M
PITT AIDS RESEARCH TRAINING PROGRAMT32AI065380 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BARRATT-BOYES, SIMON M · 2005 to 2020
$3.2M
TRAINING IN HIV/AIDS AT PITT--THE SHARP PROGRAMT32AI007487 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI RINALDO, CHARLES R · 1994 to 1998
–
NIAID NIH HHS P01 AI057005NIAID NIH HHS R37 AI041870NIAID NIH HHS R37 AI-41870NIAID NIH HHS T32 AI007487NIAID NIH HHS T32 AI-065380NIAID NIH HHS T32 AI065380NIAID NIH HHS U01 AI035041NIAID NIH HHS U01 AI-35041
6 · The paper itself

Abstract

The ability of HIV-1 to rapidly accumulate mutations provides the virus with an effective means of escaping CD8(+) CTL responses. In this study, we describe how subtle alterations in CTL epitopes expressed by naturally occurring HIV-1 variants can result in an incomplete escape from CTL recognition, providing the virus with a selective advantage. Rather than paralyzing the CTL response, these epitope modifications selectively induce the CTL to produce proinflammatory cytokines in the absence of target killing. Importantly, instead of dampening the immune response through CTL elimination of variant Ag-expressing immature dendritic cells (DC), a positive CTL-to-DC immune feedback loop dominates whereby the immature DC differentiate into mature proinflammatory DC. Moreover, these CTL-programmed DC exhibit a superior capacity to mediate HIV-1 trans-infection of T cells. This discordant induction of CTL helper activity in the absence of killing most likely contributes to the chronic immune activation associated with HIV-1 infection, and can be used by HIV-1 to promote viral dissemination and persistence. Our findings highlight the need to address the detrimental potential of eliciting dysfunctional cross-reactive memory CTL responses when designing and implementing anti-HIV-1 immunotherapies.

Indexed as

Coculture TechniquesDendritic CellsEpitopes, T-LymphocyteFlow CytometryHIV-1HIV InfectionsHumansLymphocyte ActivationMicroscopy, Electron, ScanningT-Lymphocytes, CytotoxicEpitopes, T-Lymphocyte

Identifiers

PMID23913962
PMCPMC3786204
OpenAlexW2147039193

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.