Evidence map›Paper›PMID 30019620›Full record

ArticleCell cycle (Georgetown, Tex.)2018

An engineered novel lentivector specifically transducing dendritic cells and eliciting robust HBV-specific CTL response by upregulating autophagy in T cells.

Siyuan Ma, Xiaohua Chen, Quanhui Tan, Dan Li, Shenglan Dai, Shanshan Wu, Yongsheng Yu, Guoqing Zang, Zhenghao Tang

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
0.2field-weighted citation impact, top 45% 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

3 citing papers in PubMed, 1 synthesis or guideline pooled it, 6 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. 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 2 institutions in 1 country.

Siyuan Maa Department of Infectious Disease , Shanghai Jiao Tong University Affiliated Sixth People's Hospital , Shanghai , China.
Xiaohua Chena Department of Infectious Disease , Shanghai Jiao Tong University Affiliated Sixth People's Hospital , Shanghai , China.
Quanhui Tana Department of Infectious Disease , Shanghai Jiao Tong University Affiliated Sixth People's Hospital , Shanghai , China.
Dan Lia Department of Infectious Disease , Shanghai Jiao Tong University Affiliated Sixth People's Hospital , Shanghai , China.
Shenglan Daia Department of Infectious Disease , Shanghai Jiao Tong University Affiliated Sixth People's Hospital , Shanghai , China.
Shanshan Wua Department of Infectious Disease , Shanghai Jiao Tong University Affiliated Sixth People's Hospital , Shanghai , China.
Yongsheng Yua Department of Infectious Disease , Shanghai Jiao Tong University Affiliated Sixth People's Hospital , Shanghai , China.
Guoqing Zanga Department of Infectious Disease , Shanghai Jiao Tong University Affiliated Sixth People's Hospital , Shanghai , China.
Zhenghao Tanga Department of Infectious Disease , Shanghai Jiao Tong University Affiliated Sixth People's Hospital , Shanghai , China.
Shanghai Jiao Tong University · CNShanghai Sixth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dendritic cells (DCs) play a predominant role in initiating cell immune responses. Here we generated a DC-targeting lentiviral vector (LVDC-UbHBcAg-LIGHT) and evaluated its capacity to elicit HBV-specific cytotoxic T lymphocyte (CTL) responses. DC-SIGN-mediated specific transduction using this construct was confirmed in DC-SIGN-expressing 293T cells and ex vivo-cultured bone marrow cells. LVDC-UbHBcAg-LIGHT-loaded DCs were highly effective in inducing HBV-specific CTLs. Mechanistic studies demonstrated autophagy blocking led to a significant increase in apoptosis and obvious inhibition of CD8 + T cells entry into S-phase, correspondingly attenuated LVDC-UbHBcAg-LIGHT-loaded DC-induced T cell responses. This observation was supported by accumulation of pro-apoptotic proteins and the main negative cell cycle regulator-CDKN1B that otherwise would be degraded in activated T cells where autophagy preferentially occured. Our findings revealed an important role of autophagy in the activation of T cells and suggested LVDC-UbHBcAg-LIGHT may potentially be used as a therapeutic strategy to combat persistent HBV infection with higher security.

Indexed as

AutophagyTransduction, GeneticUp-RegulationAdenineAnimalsApoptosisAutophagy-Related Protein 5CD8-Positive T-LymphocytesCell Adhesion MoleculesDC-Specific ICAM-3 Grabbing NonintegrinDendritic CellsGenetic EngineeringGenetic VectorsHepatitis B Core AntigensHepatitis B virusHumans3-methyladenineAdenineAutophagy-Related Protein 5Cell Adhesion MoleculesDC-Specific ICAM-3 Grabbing NonintegrinHepatitis B Core AntigensLectins, C-TypeReceptors, Cell SurfaceTumor Necrosis Factor Ligand Superfamily Member 14Ubiquitinautophagycytotoxic T lymphocyte (CTL)Dendritic cell (DC)-targeting lentivector

Identifiers

PMID30019620
PMCPMC6110602
OpenAlexW2884767312

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.