Evidence map›Paper›PMID 22210916›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

Clonotype and repertoire changes drive the functional improvement of HIV-specific CD8 T cell populations under conditions of limited antigenic stimulation.

Loury Janbazian, David A Price, Glenda Canderan, Abdelali Filali-Mouhim, Tedi E Asher, David R Ambrozak, Phillip Scheinberg, Mohamad Rachid Boulassel, Jean-Pierre Routy, Richard A Koup and 3 more

Registry-linked trialAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02208167 (IGHID 1320 - A Phase I Study to Evaluate the Safety, Immunologic, and Virologic Responses of HIV-1 Antigen Expanded Specific T Cell Therapy), which is not on this map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
–field-weighted citation impact
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.

NCT02208167 phase1completednot on this mapstarted 2015, after this paper: background citation

IGHID 1320 - A Phase I Study to Evaluate the Safety, Immunologic, and Virologic Responses of HIV-1 Antigen Expanded Specific T Cell Therapy (HXTC) as a Therapeutic Strategy in HIV-Infected Individuals Started on Antiretroviral Therapy During Acute and Chronic Infection

TypeinterventionalSponsorUniversity of North Carolina, Chapel HillRan2015 to 2017Enrolled6ConditionsHIVArmsHXTC infusion
3 · Its place in the literature

Who cites it

33 citing papers in PubMed.

  1. Article
  2. Observational
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. A Fixed Spatial Structure of CD8Journal of immunology (Baltimore, Md. : 1950) · 2018
    Article
  11. Clonally diverse CD38Nature communications · 2018
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Delayed differentiation of potent effector CD8Science translational medicine · 2017
    Article
  17. Kill: boosting HIV-specific immune responses.Current opinion in HIV and AIDS · 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

13 authors.

Loury JanbazianLaboratory of Immunology, Department of Microbiology and Immunology, University of Montreal, Montreal, Quebec H2X 1P1, Canada.
David A Price
Glenda Canderan
Abdelali Filali-Mouhim
Tedi E Asher
David R Ambrozak
Phillip Scheinberg
Mohamad Rachid Boulassel
Jean-Pierre Routy
Richard A Koup
Daniel C Douek
Rafick-Pierre Sekaly
Lydie Trautmann

Funding

Testing of Blood Samples for Immune Response and Vaccine ResearchZIAAI005073 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI KOUP, RICHARD A · 2009 to 2025
$23.4M
Novel Concepts for the Eradication of HIVDP1DA028871 · NIDA · VGTI FLORIDA · PI SEKALY, RAFICK PIERRE · 2009 to 2013
$4.5M
CIHRMedical Research Council G0501963NIDA NIH HHS DP1 DA028871PHS HHS IDPIDA028871-01
6 · The paper itself

Abstract

Persistent exposure to cognate Ag leads to the functional impairment and exhaustion of HIV-specific CD8 T cells. Ag withdrawal, attributable either to antiretroviral treatment or the emergence of epitope escape mutations, causes HIV-specific CD8 T cell responses to wane over time. However, this process does not continue to extinction, and residual CD8 T cells likely play an important role in the control of HIV replication. In this study, we conducted a longitudinal analysis of clonality, phenotype, and function to define the characteristics of HIV-specific CD8 T cell populations that persist under conditions of limited antigenic stimulation. Ag decay was associated with dynamic changes in the TCR repertoire, increased expression of CD45RA and CD127, decreased expression of programmed death-1, and the emergence of polyfunctional HIV-specific CD8 T cells. High-definition analysis of individual clonotypes revealed that the Ag loss-induced gain of function within HIV-specific CD8 T cell populations could be attributed to two nonexclusive mechanisms: 1) functional improvement of persisting clonotypes; and 2) recruitment of particular clonotypes endowed with superior functional capabilities.

Indexed as

Antigens, ViralCD8-Positive T-LymphocytesClone CellsGene Expression RegulationHIVHumansInterleukin-7 Receptor alpha SubunitLeukocyte Common AntigensLongitudinal StudiesProgrammed Cell Death 1 ReceptorAntigens, ViralInterleukin-7 Receptor alpha SubunitLeukocyte Common AntigensPDCD1 protein, humanProgrammed Cell Death 1 Receptor

Identifiers

PMID22210916
PMCPMC3262882

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Registered trials

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.