Evidence map›Paper›PMID 19949061›Full record

ArticleAntimicrobial agents and chemotherapy2010

Chloroquine modulates HIV-1-induced plasmacytoid dendritic cell alpha interferon: implication for T-cell activation.

Jeffrey A Martinson, Carlos J Montoya, Xiomara Usuga, Rollie Ronquillo, Alan L Landay, Seema N Desai

Open access · greenAbstract read
In one paragraph

Article in Antimicrobial agents and chemotherapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.

  1. Pooled it
  2. Chloroquine use improves dengue-related symptoms.Memorias do Instituto Oswaldo Cruz · 2013
    Trial
  3. Trial
  4. Trial
  5. Article
  6. Review
  7. Review
  8. Article
  9. 4-Aminoquinoline compounds from the Spanish flu to COVID-19.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021
    Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  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

6 authors at 2 institutions in 2 countries.

Jeffrey A MartinsonDepartment of Immunology and Microbiology, Rush University Medical Center, 1735 West Harrison St. (Cohn Research Building, Lab 641), Chicago, IL 60612, USA.
Carlos J Montoya
Xiomara Usuga
Rollie Ronquillo
Alan L Landay
Seema N Desai
Rush University Medical Center · USUniversidad de Antioquia · CO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Plasmacytoid dendritic cells (pDC) contribute to antiviral immunity mainly through recognition of microbial products and viruses via intracellular Toll-like receptor 7 (TLR7) or TLR9, resulting in the production of type I interferons (IFNs). Although interferons reduce the viral burden in the acute phase of infection, their role in the chronic phase is unclear. The presence of elevated plasma IFN-alpha levels in advanced HIV disease and its association with microbial translocation in chronic HIV infection lead us to hypothesize that IFN-alpha could contribute to immune activation. Blocking of IFN-alpha production using chloroquine, an endosomal inhibitor, was tested in a novel in vitro model system with the aim of characterizing the effects of chloroquine on HIV-1-mediated TLR signaling, IFN-alpha production, and T-cell activation. Our results indicate that chloroquine blocks TLR-mediated activation of pDC and MyD88 signaling, as shown by decreases in the levels of the downstream signaling molecules IRAK-4 and IRF-7 and by inhibition of IFN-alpha synthesis. Chloroquine decreased CD8 T-cell activation induced by aldrithiol-2-treated HIV-1 in peripheral blood mononuclear cell cultures. In addition to blocking pDC activation, chloroquine also blocked negative modulators of the T-cell response, such as indoleamine 2,3-dioxygenase (IDO) and programmed death ligand 1 (PDL-1). Our results indicate that TLR stimulation and production of IFN-alpha by pDC contribute to immune activation and that blocking of these pathways using chloroquine may interfere with events contributing to HIV pathogenesis. Our results suggests that a safe, well-tolerated drug such as chloroquine can be proposed as an adjuvant therapeutic candidate along with highly active antiretroviral therapy to control immune activation in HIV-1 infection.

Indexed as

Antigens, CDAnti-HIV AgentsApoptosis Regulatory ProteinsCells, CulturedChloroquineDendritic CellsEnzyme ActivationFlow CytometryHIV-1HumansIndoleamine-Pyrrole 2,3,-DioxygenaseInterferon-alphaLymphocyte ActivationProgrammed Cell Death 1 ReceptorT-LymphocytesToll-Like Receptor 7Antigens, CDAnti-HIV AgentsApoptosis Regulatory ProteinsChloroquineIndoleamine-Pyrrole 2,3,-DioxygenaseInterferon-alphaPDCD1 protein, humanProgrammed Cell Death 1 ReceptorTLR7 protein, humanToll-Like Receptor 7

Identifiers

PMID19949061
PMCPMC2812138
OpenAlexW2146674508

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.