Evidence map›Paper›PMID 33089108›Full record

ArticleiScience2020

Δ42PD1-TLR4 Augments γδ-T Cell Activation of the Transitional Memory Subset of CD4

Yufei Mo, Allen Ka Loon Cheung, Yue Liu, Li Liu, Zhiwei Chen

Open access · goldAbstract read
In one paragraph

Article in iScience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 40% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Yufei MoAIDS Institute and Department of Microbiology, State Key Laboratory of Emerging Infectious Diseases, Li Ka Shing Faculty of Medicine, The University of Hong Kong, L5-45, 21 Sassoon Road, Pokfulam, Hong Kong SAR, China.
Allen Ka Loon CheungDepartment of Biology, Faculty of Science, RRS833, Ho Sin-hang Campus, Hong Kong Baptist University, 224 Waterloo Road, Kowloon Tong, Hong Kong SAR, China.
Yue LiuDepartment of Biology, Faculty of Science, RRS833, Ho Sin-hang Campus, Hong Kong Baptist University, 224 Waterloo Road, Kowloon Tong, Hong Kong SAR, China.
Li LiuAIDS Institute and Department of Microbiology, State Key Laboratory of Emerging Infectious Diseases, Li Ka Shing Faculty of Medicine, The University of Hong Kong, L5-45, 21 Sassoon Road, Pokfulam, Hong Kong SAR, China.
Zhiwei ChenAIDS Institute and Department of Microbiology, State Key Laboratory of Emerging Infectious Diseases, Li Ka Shing Faculty of Medicine, The University of Hong Kong, L5-45, 21 Sassoon Road, Pokfulam, Hong Kong SAR, China.
University of Hong Kong · HKHong Kong Baptist University · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TLR ligands can contribute to T cell immune responses by indirectly stimulating antigen presentation and cytokines and directly serving as co-stimulatory signals. We have previously reported that the human endogenous surface protein, Δ42PD1, is expressed primarily on (Vγ9)Vδ2 cells and can interact with TLR4. Since Vδ2 cells possess antigen presentation capacity, we sought to further characterize if the Δ42PD1-TLR4 interaction has a role in stimulating T cell responses. In this study, we found that stimulation of Vδ2 cells not only upregulated Δ42PD1 expression but also increased MHC class II molecules necessary for the antigen presentation. In a mixed leukocyte reaction assay, upregulation of Δ42PD1 on Vδ2 cells elevated subsequent T cell proliferation. Furthermore, the interaction between Δ42PD1-TLR4 augments Vδ2 cell stimulation of autologous CMV pp65-or TT-specific CD4

Indexed as

Cell BiologyImmunology

Identifiers

PMID33089108
PMCPMC7567942
OpenAlexW3088793496

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.