Evidence map›Paper›PMID 27531999›Full record

ReviewFrontiers in immunology2016

Insights into Soluble Toll-Like Receptor 2 as a Downregulator of Virally Induced Inflammation.

Bethany M Henrick, Xiao-Dan Yao, Ameer Y Taha, J Bruce German, Kenneth Lee Rosenthal

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

29 citing papers in PubMed, 48 citations in OpenAlex.

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  4. Redefinition of the toll-like receptor repertoire inFrontiers in cellular and infection microbiology · 2025
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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 2 countries.

Bethany M HenrickFood Science and Technology, Foods for Health Institute, University of California Davis , Davis, CA , USA.
Xiao-Dan YaoDepartment of Pathology and Molecular Medicine, McMaster Immunology Research Centre, Michael G. DeGroote Institute for Infectious Disease Research, McMaster University , Hamilton, ON , Canada.
Ameer Y TahaFood Science and Technology, Foods for Health Institute, University of California Davis , Davis, CA , USA.
J Bruce GermanFood Science and Technology, Foods for Health Institute, University of California Davis , Davis, CA , USA.
Kenneth Lee RosenthalDepartment of Pathology and Molecular Medicine, McMaster Immunology Research Centre, Michael G. DeGroote Institute for Infectious Disease Research, McMaster University , Hamilton, ON , Canada.
University of California, Davis · USMcMaster University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ability to distinguish pathogens from self-antigens is one of the most important functions of the immune system. However, this simple self versus non-self assignment belies the complexity of the immune response to threats. Immune responses vary widely and appropriately according to a spectrum of threats and only recently have the mechanisms for controlling this highly textured process emerged. A primary mechanism by which this controlled decision-making process is achieved is via Toll-like receptor (TLR) signaling and the subsequent activation of the immune response coincident with the presence of pathogenic organisms or antigens, including lipid mediators. While immune activation is important, the appropriate regulation of such responses is also critical. Recent findings indicate a parallel pathway by which responses to both viral and bacterial infections is controlled via the secretion of soluble TLR2 (sTLR2). sTLR2 is able to bind a wide range of pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs). sTLR2 has been detected in many bodily fluids and is thus ubiquitous in sites of pathogen appearance. Interestingly, growing evidence suggests that sTLR2 functions to sequester PAMPs and DAMPs to avoid immune activation via detection of cellular-expressed TLRs. This immune regulatory function would serve to reduce the expression of the molecules required for cellular entry, and the recruitment of target cells following infection with bacteria and viruses. This review provides an overview of sTLR2 and the research regarding the mechanisms of its immune regulatory properties. Furthermore, the role of this molecule in regulating immune activation in the context of HIV infection via sTLR2 in breast milk provides actionable insights into therapeutic targets across a variety of infectious and inflammatory states.

Indexed as

inflammationinnate immunitymucosal fluidspathogen-associated molecular patternspattern recognition receptorssoluble TLR2toll-like receptorsviruses

Identifiers

PMID27531999
PMCPMC4969314
OpenAlexW2500944829

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.