Evidence map›Paper›PMID 34277108›Full record

ReviewImmune network2021

Toll-like Receptor 2 in Autoimmune Inflammation.

Kathryne E Marks, Kaylin Cho, Courtney Stickling, Joseph M Reynolds

Open access · diamondAbstract readReview
In one paragraph

Review in Immune network, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
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  5. Article
  6. Oral Pathobiont-Derived Outer Membrane Vesicles in the Oral-Gut Axis.International journal of molecular sciences · 2024
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Toll-Like Receptor 2 Modulates Pulmonary Inflammation and TNF-α Release Mediated byFrontiers in cellular and infection microbiology · 2022
    Article
  19. Review
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

4 authors at 1 institution in 1 country.

Kathryne E MarksCenter for Cancer Cell Biology, Immunology, and Infection, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL, USA.ORCID https://orcid.org/0000-0002-1524-7159
Kaylin ChoCenter for Cancer Cell Biology, Immunology, and Infection, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL, USA.ORCID https://orcid.org/0000-0002-0555-4761
Courtney SticklingCenter for Cancer Cell Biology, Immunology, and Infection, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL, USA.ORCID https://orcid.org/0000-0002-7353-5837
Joseph M ReynoldsCenter for Cancer Cell Biology, Immunology, and Infection, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL, USA.ORCID https://orcid.org/0000-0003-3490-0544
Rosalind Franklin University of Medicine and Science · US

Funding

Molecular regulation of TLR2-mediated autoimmune inflammationR01AI141596 · NIAID · ROSALIND FRANKLIN UNIV OF MEDICINE & SCI · PI REYNOLDS, JOSEPH MICHAEL · 2019 to 2023
$1.9M
NIAID NIH HHS R01 AI141596
6 · The paper itself

Abstract

TLR signaling is critical for broad scale immune recognition of pathogens and/or danger molecules. TLRs are particularly important for the activation and the maturation of cells comprising the innate immune response. In recent years it has become apparent that several different TLRs regulate the function of lymphocytes as well, albeit to a lesser degree compared to innate immunity. TLR2 heterodimerizes with either TLR1 or TLR6 to broadly recognize bacterial lipopeptides as well as several danger-associated molecular patterns. In general, TLR2 signaling promotes immune cell activation leading to tissue inflammation, which is advantageous for combating an infection. Conversely, inappropriate or dysfunctional TLR2 signaling leading to an overactive inflammatory response could be detrimental during sterile inflammation and autoimmune disease. This review will highlight and discuss recent research advances linking TLR2 engagement to autoimmune inflammation.

Indexed as

AutoimmunityExperimental autoimmune encephalomyelitisTh17 CellsT Lymphocytes, RegulatoryToll-like receptorToll-like receptor 2

Identifiers

PMID34277108
PMCPMC8263214
OpenAlexW3185930379

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.