Evidence map›Paper›PMID 23149661›Full record

ArticleMucosal immunology2013

Preferential depletion of gut CD4-expressing iNKT cells contributes to systemic immune activation in HIV-1 infection.

F J Ibarrondo, S B Wilson, L E Hultin, R Shih, M A Hausner, P M Hultin, P A Anton, B D Jamieson, O O Yang

Open access · bronzeAbstract read
In one paragraph

Article in Mucosal immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

21 citing papers in PubMed, 37 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Review
  5. Article
  6. Dominant CD8Frontiers in immunology · 2022
    Article
  7. Preferential and persistent impact of acute HIV-1 infection on CD4Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  8. Gut Innate Immunity and HIV Pathogenesis.Current HIV/AIDS reports · 2021
    Review
  9. Metabolomics as a Tool to Investigate HIV/TB Co-Infection.Frontiers in molecular biosciences · 2021
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
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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 1 institution in 1 country.

F J IbarrondoDepartment of Medicine and UCLA AIDS Institute, David Geffen School of Medicine at University of California Los Angeles, Los Angeles, California, USA.
S B Wilson
L E Hultin
R Shih
M A Hausner
P M Hultin
P A Anton
B D Jamieson
O O Yang
University of California, Los Angeles · US

Funding

Virology CoreP30AI028697 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MITSUYASU, RONALD T. · 1991 to 2018
$39.9M
Mucosal and Peripheral NK-T Cells in HIV InfectionR21AI063974 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI YANG, OTTO O · 2006 to 2007
$419k
NIAID NIH HHS AI028697NIAID NIH HHS AI063974NIAID NIH HHS P30 AI028697NIAID NIH HHS R21 AI063974
6 · The paper itself

Abstract

Chronic inappropriate immune activation is the central defect-driving loss of CD4(+) T helper cells and progression to AIDS in persons with HIV-1 infection, but the mechanisms remain controversial. We examined key regulatory invariant receptor natural killer T (iNKT) cells in the gut, the largest reservoir of lymphocytes and a key arena of HIV-1 pathogenesis. In healthy control persons, the anti-inflammatory CD4(+) iNKT-cell subset predominated over the pro-inflammatory CD4(-) iNKT-cell subset in the gut, but not in the blood, compartment. HIV-1 infection resulted in a preferential loss of this anti-inflammatory CD4(+) iNKT-cell subset within the gut. The degree of loss of the CD4(+) iNKT-cell subset in the gut, but not in the blood, correlated to the systemic immune activation and exhaustion that have been linked to disease progression. These results suggest a potentially important contribution of gut iNKT-cell imbalance in determining the systemic immune activation that is the hallmark of HIV-1 pathogenesis.

Indexed as

Lymphocyte DepletionAdultCD4 AntigensCell DeathDisease ProgressionHIV-1HIV InfectionsHumansImmunomodulationIntestinesLymphocyte CountMaleMiddle AgedNatural Killer T-CellsVirus ActivationYoung AdultCD4 Antigens

Identifiers

PMID23149661
PMCPMC3865278
OpenAlexW2055694058

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.