Evidence map›Paper›PMID 27183126›Full record

ArticlePloS one2016

Interaction of Toll-Like Receptors with the Molecular Chaperone Gp96 Is Essential for Its Activation of Cytotoxic T Lymphocyte Response.

Weiwei Liu, Mi Chen, Xinghui Li, Bao Zhao, Junwei Hou, Huaguo Zheng, Lipeng Qiu, Zihai Li, Songdong Meng

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

13 citing papers in PubMed, 25 citations in OpenAlex.

  1. HSP90 multi-functionality in cancer.Frontiers in immunology · 2024
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. SARS-CoV-2 Infection and Candidate Biomarkers.The Eurasian journal of medicine · 2022
    Article
  7. Article
  8. Article
  9. Article
  10. Broadly Protective CD8Journal of virology · 2021
    Article
  11. The HSP Immune Network in Cancer.Frontiers in immunology · 2021
    Review
  12. Article
  13. Article
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

9 authors at 4 institutions in 2 countries.

Weiwei LiuCAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing, P.R. China.
Mi ChenCAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing, P.R. China.
Xinghui LiCAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing, P.R. China.
Bao ZhaoCAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing, P.R. China.
Junwei HouCAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing, P.R. China.
Huaguo ZhengCAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing, P.R. China.
Lipeng QiuInstitute of Life Sciences, Jiangsu University, Zhenjiang, P.R. China.
Zihai LiDepartment of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC, United States of America.
Songdong MengCAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing, P.R. China.
Institute of Microbiology · CNChinese Academy of Sciences · CNJiangsu University · CNMedical University of South Carolina · US

Funding

Project 3: Structural Basis for grp94 Drug Development and Chaperone FunctionP01CA186866 · NCI · OHIO STATE UNIVERSITY · PI GEWIRTH, DANIEL T · 2015 to 2019
$6.7M
NCI NIH HHS P01 CA186866
6 · The paper itself

Abstract

The heat shock protein gp96 elicits specific T cell responses to its chaperoned peptides against cancer and infectious diseases in both rodent models and clinical trials. Although gp96-induced innate immunity, via a subset of Toll like receptors (TLRs), and adaptive immunity, through antigen presentation, are both believed to be important for priming potent T cell responses, direct evidence for the role of gp96-mediated TLR activation related to its functional T cell activation is lacking. Here, we report that gp96 containing mutations in its TLR-binding domain failed to activate macrophages, but peptide presentation was unaffected. Moreover, we found that peptide-specific T cell responses, as well as antitumor T cell immunity induced by gp96, are severely impaired when the TLR-binding domain is mutated. These data demonstrate the essential role of the gp96-TLR interaction in priming T cell immunity and provide further molecular basis for the coupling of gp96-mediated innate with adaptive immunity.

Indexed as

Amino Acid SequenceAnimalsAntigen PresentationCell LineCross-PrimingCytokinesEpitopes, T-LymphocyteFemaleHumansLymphocyte ActivationMacrophagesMelanoma, ExperimentalMembrane GlycoproteinsMiceMutationPeptidesCytokinesendoplasminEpitopes, T-LymphocyteMembrane GlycoproteinsPeptidesToll-Like Receptors

Identifiers

PMID27183126
PMCPMC4868323
OpenAlexW2394779300

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.