Evidence map›Paper›PMID 19430930›Full record

ReviewClinical reviews in allergy & immunology2010

The role of Toll-like receptor signaling in human immunodeficiencies.

Hanna Suhir, Amos Etzioni

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical reviews in allergy & immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

15 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Bacterial interference with canonical NFκB signalling.Microbiology (Reading, England) · 2013
    Review
  7. Article
  8. TRAF molecules in cell signaling and in human diseases.Journal of molecular signaling · 2013
    Article
  9. Article
  10. Article
  11. The future of autoimmunity.Clinical reviews in allergy & immunology · 2012
    Article
  12. Article
  13. Article
  14. Article
  15. Article
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

2 authors at 1 institution in 1 country.

Hanna SuhirMeyer's Children Hospital, The Rappaport School of Medicine, Technion, Haifa, Israel.
Amos Etzioni
Technion – Israel Institute of Technology · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Through the last decade, clinical immunology has witnessed a considerable progress in understanding the role of the innate immunity in human host defense, with Toll-like receptors (TLRs) being the most extensively innate immune receptors investigated. Growing literature documents the relevance of TLR signaling pathways to human disease, revealing a small, but expanding, group of new monogenic primary immunodeficiencies, in patients with various infectious diseases, previously considered as of unexplained "idiopathic" origin. Herein, we review these recently described deficiencies. Autosomal recessive IRAK-4 and myeloid differentiation factor 88 deficiencies were reported in 2003 and 2008, respectively, conferring predisposition to pyogenic bacterial infections, and autosomal recessive UNC93B1 and autosomal dominant TLR3 deficiencies were reported in 2006 and 2007, respectively, conferring predisposition to herpes simplex encephalitis. Furthermore, we highlight the published data associating TLR polymorphism with an altered susceptibility to infectious diseases.

Indexed as

Immunity, InnateImmunologic Deficiency SyndromesSignal TransductionToll-Like ReceptorsChildChild, PreschoolDisease SusceptibilityHumansPolymorphism, GeneticToll-Like Receptors

Identifiers

PMID19430930
OpenAlexW1968869895

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.