Evidence map›Paper›PMID 21403126›Full record

ArticleBlood2011

Epithelial adhesion molecules can inhibit HIV-1-specific CD8⁺ T-cell functions.

Hendrik Streeck, Douglas S Kwon, Augustine Pyo, Michael Flanders, Mathieu F Chevalier, Kenneth Law, Boris Jülg, Kasper Trocha, Jonathan S Jolin, Melis N Anahtar and 11 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing 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

28 citing papers in PubMed, 37 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Resident CD49aScience advances · 2026
    Article
  5. The role of KLRG1: a novel biomarker and new therapeutic target.Cell communication and signaling : CCS · 2024
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Control ofFrontiers in cellular and infection microbiology · 2022
    Article
  12. Article
  13. Article
  14. The CD8Microbiology and molecular biology reviews : MMBR · 2021
    Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review
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

21 authors at 4 institutions in 1 country.

Hendrik StreeckRagon Institute of MGH, MIT, and Harvard, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. hstreeck@partners.org
Douglas S Kwon
Augustine Pyo
Michael Flanders
Mathieu F Chevalier
Kenneth Law
Boris Jülg
Kasper Trocha
Jonathan S Jolin
Melis N Anahtar
Jeff Lian
Ildiko Toth
Zabrina Brumme
J Judy Chang
Tyler Caron
Scott J Rodig
Danny A Milner
Alicja Piechoka-Trocha
Daniel E Kaufmann
Bruce D Walker
Marcus Altfeld
Harvard University · USRagon Institute of MGH, MIT and Harvard · USBrigham and Women's Hospital · USHoward Hughes Medical Institute · US

Funding

Medical Scientist Training ProgramT32GM007753 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI WALENSKY, LOREN DAVID · 1985 to 2021
$50.0M
CTL Responses to Regulatory and Accessory HIV-1 ProteinsR01AI050429 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI ALTFELD, MARCUS · 2002 to 2011
$3.7M
Gut mucosal immunity to HIV-1 in controlled and progressive infectionK08AI084546 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI KWON, DOUGLAS · 2009 to 2012
$498k
NIAID NIH HHS K08 AI084546NIAID NIH HHS R01 AI050429NIAID NIH HHS R01-AI50429NIGMS NIH HHS T32 GM007753
6 · The paper itself

Abstract

Under persistent antigenic stimulation, virus-specific CD8⁺ T cells become increasingly dysfunctional and up-regulate several inhibitory molecules such as killer lectin-like receptor G1 (KLRG1). Here, we demonstrate that HIV-1 antigen-specific T cells from subjects with chronic-progressive HIV-1 infection have significantly elevated KLRG1 expression (P < .001); show abnormal distribution of E-cadherin, the natural ligand of KLRG1, in the intestinal mucosa; and have elevated levels of systemic soluble E-cadherin (sE-cadherin) that significantly correlate with HIV-1 viral load (R = 0.7, P = .004). We furthermore demonstrate that in the presence of sE-cadherin, KLRG1(hi) HIV-1-specific CD8⁺ T cells are impaired in their ability to respond by cytokine secretion on antigenic stimulation (P = .002) and to inhibit viral replication (P = .03) in vitro. Thus, these data suggest a critical mechanism by which the disruption of the intestinal epithelium associated with HIV-1 leads to increased systemic levels of sE-cadherin, which inhibits the effector functions of KLRG1(hi)-expressing HIV-1-specific CD8⁺ T cells systemically.

Indexed as

CadherinsCD8-Positive T-LymphocytesCell Adhesion MoleculesCell SeparationColonEnzyme-Linked Immunosorbent AssayFemaleFlow CytometryFluorescent Antibody TechniqueHIV-1HIV InfectionsHumansImmunohistochemistryLectins, C-TypeLymphocyte ActivationMaleCadherinsCell Adhesion MoleculesKLRG1 protein, humanLectins, C-TypeReceptors, ImmunologicTrans-Activators

Identifiers

PMID21403126
PMCPMC3109536
OpenAlexW2023661718

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.