Evidence map›Paper›PMID 26671458›Full record

ArticleScientific reports2015

HIV-1 increases TLR responses in human primary astrocytes.

M Jesús Serramía, M Ángeles Muñoz-Fernández, Susana Álvarez

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

24 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Alcohol, HMGB1, and Innate Immune Signaling in the Brain.Alcohol research : current reviews · 2024
    Review
  4. Involvement of lncRNA TUG1 in HIV-1 Tat-Induced Astrocyte Senescence.International journal of molecular sciences · 2023
    Article
  5. Immune Functions of Astrocytes in Viral Neuroinfections.International journal of molecular sciences · 2023
    Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Cytosolic DNA Sensors and CNS Responses to Viral Pathogens.Frontiers in cellular and infection microbiology · 2020
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. 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

3 authors at 2 institutions in 1 country.

M Jesús SerramíaLaboratorio Inmuno-Biología Molecular, Hospital General Universitario Gregorio Marañón, Madrid, Spain.
M Ángeles Muñoz-FernándezLaboratorio Inmuno-Biología Molecular, Hospital General Universitario Gregorio Marañón, Madrid, Spain.
Susana ÁlvarezLaboratorio Inmuno-Biología Molecular, Hospital General Universitario Gregorio Marañón, Madrid, Spain.
Biomedical Research Networking Center in Bioengineering, Biomaterials and Nanomedicine · ESHospital General Universitario Gregorio Marañón · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Astrocytes are the major glial cell within the central nervous system and have a number of important physiological properties related to brain homeostasis. They provide trophic support to neurons and are immune cells with key roles during states-of-inflammation. The potential for production of proinflammatory cytokines and its consequences has been studied in the context of HIV-1 infection of normal human astrocytes (NHA). NHA express TLR3, TLR4, and TLR5. TLR3 ligation induced the strongest proinflammatory polarizing response, characterized by generation of high levels of TNF-α, IL-6, and IL-8. HIV-1 increased the transient production of key inflammatory mediators, and exposure to LPS of HIV-1-infected cells increased significantly the cytokine secretion. We confirmed that it is necessary viral gene expression from the moment of pretreatment with antiretrovirals inhibited totally HIV-1-induced TLR response. The higher response to LPS from HIV-1-infected cells did not correlate with TLR4 or MyD88 increased expression. LPS responsiveness of infected cells parallels MHC class II expression, but not CD14. HIV-1-infected NHA present increased sensitivity to the proinflammatory effects of LPS. If this phenomenon occurs in vivo, it will contribute to the immunopathogenesis of this disease and may ultimately offer novel targets for immunomodulatory therapy.

Indexed as

AstrocytesCell MovementCells, CulturedCytokinesGene ExpressionHistocompatibility Antigens Class IIHIV-1HumansInflammation MediatorsLigandsLipopolysaccharide ReceptorsLipopolysaccharidesMyeloid Differentiation Factor 88NF-kappa BProtein BindingRNA, MessengerCytokinesHistocompatibility Antigens Class IIInflammation MediatorsLigandsLipopolysaccharide ReceptorsLipopolysaccharidesMyeloid Differentiation Factor 88NF-kappa BRNA, MessengerToll-Like Receptors

Identifiers

PMID26671458
PMCPMC4680863
OpenAlexW2405053100

What OpenQuestion holds

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LicenceCC BY
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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.