Evidence map›Paper›PMID 21406030›Full record

ArticleAIDS research and human retroviruses2011

Up-regulation of TLR2 and TLR4 in dendritic cells in response to HIV type 1 and coinfection with opportunistic pathogens.

Juan C Hernández, Jose Arteaga, Stéphane Paul, Ajit Kumar, Eicke Latz, Silvio Urcuqui-Inchima

Erratum issuedAbstract read
In one paragraph

Article in AIDS research and human retroviruses, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

32 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Innate Immune Response Against HIV-1.Advances in experimental medicine and biology · 2021
    Article
  9. Plasmacytoid dendritic cells in the eye.Progress in retinal and eye research · 2021
    Review
  10. Article
  11. Isolation, Transfection, and Culture of Primary Human Monocytes.Journal of visualized experiments : JoVE · 2019
    Article
  12. Observational
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

6 authors at 4 institutions in 3 countries.

Juan C HernándezGrupo Inmunovirología, Universidad de Antioquia, Medellín, Colombia. juankhernandez@gmail.com
Jose Arteaga
Stéphane Paul
Ajit Kumar
Eicke Latz
Silvio Urcuqui-Inchima
Universidad de Antioquia · COGeorge Washington University · USIndustrial University of Santander · COUniversity of Bonn · DE

Funding

HDL prevention of cholesterol crystal inflammation in HIV diseaseR01HL112661 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI FITZGERALD, MICHAEL LEO, LATZ, EICKE · 2012 to 2016
$3.1M
Inflammasome activation by cholesterol crystalsR01HL093262 · NHLBI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI LATZ, EICKE · 2009 to 2013
$2.0M
Role of PISA; a PYHIN Family Member in Intracellular DNA RecognitionR01AI083713 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI FITZGERALD, KATHERINE A., LATZ, EICKE · 2009 to 2013
$2.0M
NHLBI NIH HHS R01 HL093262NHLBI NIH HHS R01 HL112661NIAID NIH HHS R01 AI083713
6 · The paper itself

Abstract

The ability to trigger an innate immune response against opportunistic pathogens associated with HIV-1 infection is an important aspect of AIDS pathogenesis. Toll-like receptors (TLRs) play a critical role in innate immunity against pathogens, but in HIV-1 patients coinfected with opportunistic infections, the regulation of TLR expression has not been studied. In this context, we have evaluated the expression of TLR2 and TLR4 in monocytes, plasmacytoid dendritic cells, and myeloid dendritic cells of HIV-1 patients with or without opportunistic infections. Forty-nine HIV-1-infected individuals were classified according to viral load, highly active antiretroviral therapy (HAART), and the presence or absence of opportunistic infections, and 21 healthy subjects served as controls. Increased expression of TLR2 and TLR4 was observed in myeloid dendritic cells of HIV-1 patients coinfected with opportunistic infections (without HAART), while TLR4 increased in plasmacytoid dendritic cells, compared to both HIV-1 without opportunistic infections and healthy subjects. Moreover, TLR2 expression was higher in patients with opportunistic infections without HAART and up-regulation of TLR expression in HIV-1 patients coinfected with opportunistic infections was more pronounced in dendritic cells derived from individuals coinfected with Mycobacterium tuberculosis. The results indicate that TLR expression in innate immune cells is up-regulated in patients with a high HIV-1 load and coinfected with opportunistic pathogens. We suggest that modulation of TLRs expression represents a mechanism that promotes HIV-1 replication and AIDS pathogenesis in patients coinfected with opportunistic pathogens.

Indexed as

CoinfectionAdultAIDS-Related Opportunistic InfectionsAntiretroviral Therapy, Highly ActiveBacterial InfectionsCandidaCandidiasisCase-Control StudiesCD4 Lymphocyte CountDendritic CellsFemaleFlow CytometryGene Expression RegulationHIV-1HIV InfectionsHumansRNA, MessengerRNA, ViralTLR2 protein, humanTLR4 protein, humanToll-Like Receptor 2Toll-Like Receptor 4

Identifiers

PMID21406030
PMCPMC3482873
OpenAlexW1964051100

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.