Evidence map›Paper›PMID 21115690›Full record

ArticleThe Journal of experimental medicine2010

Preferential infection and depletion of Mycobacterium tuberculosis-specific CD4 T cells after HIV-1 infection.

Christof Geldmacher, Njabulo Ngwenyama, Alexandra Schuetz, Constantinos Petrovas, Klaus Reither, Edwin J Heeregrave, Joseph P Casazza, David R Ambrozak, Mark Louder, William Ampofo and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 144 papers.

0numbers the graph read from it
0cells of the map it votes in
144citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

144 citing papers in PubMed, 235 citations in OpenAlex.

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  10. HCV-specific CD4EBioMedicine · 2026
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84 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

19 authors at 6 institutions in 5 countries.

Christof GeldmacherImmunology Laboratory, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. geldmacher@lrz.uni-muenchen.de
Njabulo Ngwenyama
Alexandra Schuetz
Constantinos Petrovas
Klaus Reither
Edwin J Heeregrave
Joseph P Casazza
David R Ambrozak
Mark Louder
William Ampofo
Georgios Pollakis
Brenna Hill
Erica Sanga
Elmar Saathoff
Leonard Maboko
Mario Roederer
William A Paxton
Michael Hoelscher
Richard A Koup
National Institute for Medical Research · TZNational Institutes of Health · USNational Institute of Allergy and Infectious Diseases · USUniversity of Amsterdam · NLInstitute of Immunology · HRUniversity of Ghana · GH

Funding

HIV/SIV Replication In VivoZIAAI005014 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI KOUP, RICHARD A · 2009 to 2025
$22.7M
6 · The paper itself

Abstract

HIV-1 infection results in the progressive loss of CD4 T cells. In this study, we address how different pathogen-specific CD4 T cells are affected by HIV infection and the cellular parameters involved. We found striking differences in the depletion rates between CD4 T cells to two common opportunistic pathogens, cytomegalovirus (CMV) and Mycobacterium tuberculosis (MTB). CMV-specific CD4 T cells persisted after HIV infection, whereas MTB-specific CD4 T cells were depleted rapidly. CMV-specific CD4 T cells expressed a mature phenotype and produced very little IL-2, but large amounts of MIP-1β. In contrast, MTB-specific CD4 T cells were less mature, and most produced IL-2 but not MIP-1β. Staphylococcal enterotoxin B-stimulated IL-2-producing cells were more susceptible to HIV infection in vitro than MIP-1β-producing cells. Moreover, IL-2 production was associated with expression of CD25, and neutralization of IL-2 completely abrogated productive HIV infection in vitro. HIV DNA was found to be most abundant in IL-2-producing cells, and least abundant in MIP-1β-producing MTB-specific CD4 T cells from HIV-infected subjects with active tuberculosis. These data support the hypothesis that differences in function affect the susceptibility of pathogen-specific CD4 T cells to HIV infection and depletion in vivo, providing a potential mechanism to explain the rapid loss of MTB-specific CD4 T cells after HIV infection.

Indexed as

CD4 Lymphocyte CountCD4-Positive T-LymphocytesChemokine CCL4CytomegalovirusCytomegalovirus InfectionsFlow Cytometrygag Gene Products, Human Immunodeficiency VirusGene DosageHIV-1HIV InfectionsHumansImmunophenotypingInterferon-gammaInterleukin-2Leukocyte Common AntigensMycobacterium tuberculosisChemokine CCL4gag Gene Products, Human Immunodeficiency VirusInterferon-gammaInterleukin-2Leukocyte Common AntigensTumor Necrosis Factor Receptor Superfamily, Member 7

Identifiers

PMID21115690
PMCPMC3005236
OpenAlexW2150645172

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.