Evidence map›Paper›PMID 25784780›Full record

ReviewMediators of inflammation2015

Interleukin-1 as a common denominator from autoinflammatory to autoimmune disorders: premises, perils, and perspectives.

Giuseppe Lopalco, Luca Cantarini, Antonio Vitale, Florenzo Iannone, Maria Grazia Anelli, Laura Andreozzi, Giovanni Lapadula, Mauro Galeazzi, Donato Rigante

Open access · goldAbstract readReview
In one paragraph

Review in Mediators of inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

39 citing papers in PubMed, 102 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. GM-CSFCell reports · 2022
    Article
  9. Review
  10. The Involvement of Alarmins in the Pathogenesis of Sjögren's Syndrome.International journal of molecular sciences · 2022
    Review
  11. Effector memory CD4Science immunology · 2022
    Article
  12. Review
  13. Article
  14. Autoimmunity as the comet tail of COVID-19 pandemic.World journal of clinical cases · 2020
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  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

9 authors at 3 institutions in 1 country.

Giuseppe LopalcoInterdisciplinary Department of Medicine, University of Bari, Piazza Giulio Cesare 11, 70124 Bari, Italy.
Luca CantariniResearch Center of Systemic Autoimmune and Autoinflammatory Diseases, University of Siena, Viale Bracci 1, 53100 Siena, Italy.
Antonio VitaleResearch Center of Systemic Autoimmune and Autoinflammatory Diseases, University of Siena, Viale Bracci 1, 53100 Siena, Italy.
Florenzo IannoneInterdisciplinary Department of Medicine, University of Bari, Piazza Giulio Cesare 11, 70124 Bari, Italy.
Maria Grazia AnelliInterdisciplinary Department of Medicine, University of Bari, Piazza Giulio Cesare 11, 70124 Bari, Italy.
Laura AndreozziInstitute of Pediatrics, Università Cattolica del Sacro Cuore, Largo Agostino Gemelli 8, 00168 Rome, Italy.
Giovanni LapadulaInterdisciplinary Department of Medicine, University of Bari, Piazza Giulio Cesare 11, 70124 Bari, Italy.
Mauro GaleazziResearch Center of Systemic Autoimmune and Autoinflammatory Diseases, University of Siena, Viale Bracci 1, 53100 Siena, Italy.
Donato RiganteInstitute of Pediatrics, Università Cattolica del Sacro Cuore, Largo Agostino Gemelli 8, 00168 Rome, Italy.
University of Bari Aldo Moro · ITUniversity of Siena · ITUniversità Cattolica del Sacro Cuore · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A complex web of dynamic relationships between innate and adaptive immunity is now evident for many autoinflammatory and autoimmune disorders, the first deriving from abnormal activation of innate immune system without any conventional danger triggers and the latter from self-/non-self-discrimination loss of tolerance, and systemic inflammation. Due to clinical and pathophysiologic similarities giving a crucial role to the multifunctional cytokine interleukin-1, the concept of autoinflammation has been expanded to include nonhereditary collagen-like diseases, idiopathic inflammatory diseases, and metabolic diseases. As more patients are reported to have clinical features of autoinflammation and autoimmunity, the boundary between these two pathologic ends is becoming blurred. An overview of monogenic autoinflammatory disorders, PFAPA syndrome, rheumatoid arthritis, type 2 diabetes mellitus, uveitis, pericarditis, Behçet's disease, gout, Sjögren's syndrome, interstitial lung diseases, and Still's disease is presented to highlight the fundamental points that interleukin-1 displays in the cryptic interplay between innate and adaptive immune systems.

Indexed as

Adaptive ImmunityAnimalsAutoimmune DiseasesAutoimmunityHereditary Autoinflammatory DiseasesHumansInterleukin-1Interleukin-1

Identifiers

PMID25784780
PMCPMC4345261
OpenAlexW1996460626

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.