Evidence map›Paper›PMID 26754352›Full record

ArticleScientific reports2016

Signaling through NOD-2 and TLR-4 Bolsters the T cell Priming Capability of Dendritic cells by Inducing Autophagy.

Nargis Khan, Aurobind Vidyarthi, Susanta Pahari, Shikha Negi, Mohammad Aqdas, Sajid Nadeem, Tapan Agnihotri, Javed N Agrewala

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 49 citations in OpenAlex.

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  12. Cumulative Signaling Through NOD-2 and TLR-4 Eliminates theFrontiers in cellular and infection microbiology · 2021
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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

8 authors at 1 institution in 1 country.

Nargis KhanCSIR-Institute of Microbial Technology, Chandigarh-160036, India.
Aurobind VidyarthiCSIR-Institute of Microbial Technology, Chandigarh-160036, India.
Susanta PahariCSIR-Institute of Microbial Technology, Chandigarh-160036, India.
Shikha NegiCSIR-Institute of Microbial Technology, Chandigarh-160036, India.
Mohammad AqdasCSIR-Institute of Microbial Technology, Chandigarh-160036, India.
Sajid NadeemCSIR-Institute of Microbial Technology, Chandigarh-160036, India.
Tapan AgnihotriCSIR-Institute of Microbial Technology, Chandigarh-160036, India.
Javed N AgrewalaCSIR-Institute of Microbial Technology, Chandigarh-160036, India.
Institute of Microbial Technology · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

T cells play a cardinal role in mediating protection against intracellular pathogens like Mycobacterium tuberculosis (Mtb). It is important to understand the factors that govern the T cell response; thereby can modulate its activity. Dendritic cells (DCs) are the major player in initiation and augmentation of T cell response. Targeting DCs to induce their optimum maturation and activation can lead to a better T cell response. Interestingly, we observed that combinatorial signaling of DCs through NOD-2 and TLR-4 fortified better yield of IL-12p40/70, IL-6 and IFN-γ and upregulated the expression of CD40, CD80 and CD86 costimulatory molecules. Further, we noticed improved phagocytic capabilities of DCs. Furthermore, NOD-2 and TLR-4 induced autophagy in DCs, which enhanced the activation of T cells. This study signifies that NOD-2 and TLR-4 exhibit synergism in invigorating the activity of DCs. Consequently, this strategy may have significant immunotherapeutic potential in bolstering the function of DCs and thus improving the immunity against pathogens.

Indexed as

AutophagyCross-PrimingSignal TransductionAnimalsCell DifferentiationCytokinesDendritic CellsMice, Inbred C57BLNod2 Signaling Adaptor ProteinPhagocytosisT-LymphocytesToll-Like Receptor 4CytokinesNod2 Signaling Adaptor ProteinToll-Like Receptor 4

Identifiers

PMID26754352
PMCPMC4709561
OpenAlexW2235348035

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.