Evidence map›Paper›PMID 26159672›Full record

ReviewSeminars in immunopathology2015

Role of innate immune system in systemic sclerosis.

Nicola Fullard, Steven O'Reilly

Abstract readReview
PubMed Publisher
In one paragraph

Review in Seminars in immunopathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

36 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Emerging therapeutic targets in systemic sclerosis.Journal of molecular medicine (Berlin, Germany) · 2024
    Review
  5. Article
  6. Upcoming treatments for morphea.Immunity, inflammation and disease · 2021
    Review
  7. Review
  8. [Application of lymphocytes test in peripheral blood of patients with systemic sclerosis during the treatment].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2021
    Article
  9. Article
  10. Review
  11. Innate immunity in systemic sclerosis.Clinical and experimental immunology · 2020
    Article
  12. Article
  13. Prokineticin 2Frontiers in immunology · 2020
    Article
  14. The immunopathogenesis of fibrosis in systemic sclerosis.Clinical and experimental immunology · 2019
    Review
  15. Review
  16. Review
  17. Targeting the TLR4-MD2 axis in systemic sclerosis.Nature reviews. Rheumatology · 2018
    Article
  18. The ubiquitin proteasome system as a potential therapeutic target for systemic sclerosis.Translational research : the journal of laboratory and clinical medicine · 2018
    Review
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Nicola FullardSchool of Biological and Biomedical Sciences, Durham University, South Road, Durham, DH3, UK.
Steven O'Reilly
Durham University · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recognition of microbial or viral compounds is crucial to elicit an immune response and pattern recognition receptors (PRRs) form the first line of defence. An important family of PRRs are the Toll-like receptors (TLRs) with numerous evidences indicating their crucial role in identifying microbial or viral compounds. However, the danger theory, where the innate immune system responds to danger signals such as proteins released during damage or necrosis rather than only non-self is gaining ground. Indeed, TLRs are able to recognise endogenous molecules and have been implicated as key players in numerous autoimmune diseases including systemic sclerosis (SSc). TLR2 is known to be upregulated in SSc and has been shown to respond to the endogenous ligand amyloid A resulting in increased IL-6 secretion. TLR4 is now known to respond to a variety of endogenous ligands including fibronectin, containing alternatively spliced exons encoding type III repeat extra domain (EDA). EDA is only expressed upon tissue damage, and elevated levels can be found in SSc patients, idiopathic pulmonary fibrosis and cardiac allograft fibrosis, while deletion of EDA or TLR4 in mice reduces their fibrotic response. Further, stimulation of TLR8 with single-stranded RNA leads to increased expression of TIMP-1. This has been shown to require both IRAK4 and NF-κB with evidence suggesting autoantibodies bind to RNA to stimulate TIMP-1 production in monocytes. Therefore, TLR-mediated signalling provides numerous potential therapeutic targets for development of therapies for the treatment of multi-systemic autoimmune diseases.

Indexed as

AutoantibodiesHumansImmunity, InnateReceptors, Pattern RecognitionScleroderma, SystemicSignal TransductionToll-Like ReceptorsAutoantibodiesReceptors, Pattern RecognitionToll-Like Receptors

Identifiers

PMID26159672
OpenAlexW2252424924

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.