Evidence map›Paper›PMID 19234187›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2009

Reversal of human papillomavirus-specific T cell immune suppression through TLR agonist treatment of Langerhans cells exposed to human papillomavirus type 16.

Laura M Fahey, Adam B Raff, Diane M Da Silva, W Martin Kast

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2009. 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
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

24 citing papers in PubMed, 48 citations in OpenAlex.

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  14. Immunostimulatory Activity of the Cytokine-Based Biologic, IRX-2, on Human Papillomavirus-Exposed Langerhans Cells.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2016
    Article
  15. Human papillomavirus-exposed Langerhans cells are activated by stabilized Poly-I:C.Papillomavirus research (Amsterdam, Netherlands) · 2015
    Article
  16. 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

4 authors at 3 institutions in 3 countries.

Laura M FaheyDepartment of Molecular Microbiology & Immunology, University of Southern California, Los Angeles, CA 90033, USA.
Adam B Raff
Diane M Da Silva
W Martin Kast
University of Southern California · USCenter of Molecular Immunology (Cuba) · CUDepartment of Disease Control · TH

Funding

VLP VACCINES AGAINST HPV INDUCED TUMORSR01CA074397 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI KAST, WIJBE MARTIN · 1997 to 2020
$5.5M
Training in Genetic, Molecular and Cellular BiologyT32GM067587 · NIGMS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI STALLCUP, MICHAEL R · 2003 to 2012
$1.8M
VIROLOGY, IMMUNOLOGY &ONCOLOGY: MECHANISMS OF DISEASET32AI007078 · NIAID · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LAI, MICHAEL M.C. · 1985 to 2006
$1.1M
NCI NIH HHS R01 CA074397NCI NIH HHS R01 CA 74397NIAID NIH HHS T32 AI007078NIAID NIH HHS T32 AI07078NIGMS NIH HHS T32 GM0607587NIGMS NIH HHS T32 GM067587
6 · The paper itself

Abstract

Human papillomavirus (HPV) type 16 infects the epithelial layer of cervical mucosa and is causally associated with the generation of cervical cancer. Langerhans cells (LC) are the resident APCs at the site of infection and therefore are responsible for initiating an immune response against HPV16. On the contrary, LC exposed to HPV16 do not induce a specific T cell immune response, which leads to the immune evasion of HPV16. Demonstrating that TLR7 and TLR8 are expressed on human LC, we hypothesized that imidazoquinolines would activate LC exposed to HPV16, leading to the induction of an HPV16-specific cell-mediated immune response. Surprisingly, both phenotypic and functional hallmarks of activation are not observed when LC are exposed to HPV16 virus-like particles and treated with imiquimod (TLR7 agonist). However, we found that LC are activated by 3M-002 (TLR8 agonist) and resiquimod (TLR8/7 agonist). LC exposed to HPV16 virus-like particles and subsequently treated with 3M-002 or resiquimod highly up-regulate surface activation markers, secrete proinflammatory cytokines and chemokines, induce CCL21-directed migration, and initiate an HPV16-specific CD8(+) T cell response. These data strongly indicate that 3M-002 and resiquimod are promising therapeutics for treatment of HPV infections and HPV-induced cervical lesions.

Indexed as

Immunosuppressive AgentsAdjuvants, ImmunologicAminoquinolinesAntineoplastic AgentsCells, CulturedEpitopes, T-LymphocyteFemaleHuman papillomavirus 16HumansImidazolesImiquimodImmunity, CellularLangerhans CellsPapillomavirus InfectionsQuinolinesT-Lymphocytes3M 002Adjuvants, ImmunologicAminoquinolinesAntineoplastic AgentsEpitopes, T-LymphocyteImidazolesImiquimodImmunosuppressive AgentsQuinolinesresiquimodTLR7 protein, humanTLR8 protein, humanToll-Like Receptor 7Toll-Like Receptor 8

Identifiers

PMID19234187
PMCPMC2745289
OpenAlexW1486874809

What OpenQuestion holds

Textmetadata
LicenceTDM
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.