Evidence map›Paper›PMID 31336122›Full record

ReviewLife sciences2019

TLRs in pulmonary diseases.

Shweta Arora, Shaniya Ahmad, Rasha Irshad, Yamini Goyal, Sahar Rafat, Neha Siddiqui, Kapil Dev, Mohammad Husain, Shakir Ali, Anant Mohan and 1 more

Open access · bronzeAbstract readReview
In one paragraph

Review in Life sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

59 citing papers in PubMed, 107 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

11 authors at 4 institutions in 1 country.

Shweta AroraDepartment of Biotechnology, Jamia Millia Islamia, New Delhi, India. Electronic address: shweta169213@st.jmi.ac.in.
Shaniya AhmadDepartment of Biotechnology, Jamia Millia Islamia, New Delhi, India. Electronic address: shaniya169053@st.jmi.ac.in.
Rasha IrshadDepartment of Biotechnology, Jamia Millia Islamia, New Delhi, India. Electronic address: rasha.irshad@yahoo.com.
Yamini GoyalDepartment of Biotechnology, Jamia Millia Islamia, New Delhi, India. Electronic address: yamini188673@st.jmi.ac.in.
Sahar RafatDepartment of Biotechnology, Jamia Millia Islamia, New Delhi, India. Electronic address: saharrafat18@gmail.com.
Neha SiddiquiDepartment of Biotechnology, Jamia Millia Islamia, New Delhi, India. Electronic address: biotechnology.jamia@gmail.com.
Kapil DevDepartment of Biotechnology, Jamia Millia Islamia, New Delhi, India. Electronic address: kdev@jmi.ac.in.
Mohammad HusainDepartment of Biotechnology, Jamia Millia Islamia, New Delhi, India. Electronic address: mhusain2@jmi.ac.in.
Shakir AliDepartment of Biochemistry, School of Chemical and Life Sciences, Jamia Hamdard, New Delhi, India. Electronic address: sali@jamiahamdard.ac.in.
Anant MohanDepartment of Pulmonary Medicine, AIIMS, New Delhi, India. Electronic address: anantmohan@yahoo.com.
Mansoor Ali SyedDepartment of Biotechnology, Jamia Millia Islamia, New Delhi, India. Electronic address: smansoor@jmi.ac.in.
Department of Biotechnology · INJamia Millia Islamia · INAll India Institute of Medical Sciences · INJamia Hamdard · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Toll-like receptors (TLRs) comprise a clan of proteins involved in identification and triggering a suitable response against pathogenic attacks. As lung is steadily exposed to multiple infectious agents, antigens and host-derived danger signals, the inhabiting stromal and myeloid cells of the lung express an aggregate of TLRs which perceive the endogenously derived damage-associated molecular patterns (DAMPs) along with pathogen associated molecular patterns (PAMPs) and trigger the TLR-associated signalling events involved in host defence. Thus, they form an imperative component of host defence activation in case of microbial infections as well as non-infectious pulmonary disorders such as interstitial lung disease, acute lung injury and airways disease, such as COPD and asthma. They also play an equally important role in lung cancer. Targeting the TLR signalling network would pave ways to the design of more reliable and effective vaccines against infectious agents and control deadly infections, desensitize allergens and reduce inflammation. Moreover, TLR agonists may act as adjuvants by increasing the efficiency of cancer vaccines, thereby contributing their role in treatment of lung cancer too. Overall, TLRs present a compelling and expeditiously bolstered area of research and addressing their signalling events would be of significant use in pulmonary diseases.

Indexed as

AnimalsHumansLung DiseasesSignal TransductionToll-Like ReceptorsToll-Like ReceptorsAsthmaCOPDDAMPsLung interstitial diseasesPAMPsToll-like receptors (TLRs)

Identifiers

PMID31336122
PMCPMC7094289
OpenAlexW2963707514

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.