Evidence map›Paper›PMID 20671522›Full record

ReviewCurrent opinion in rheumatology2010

Monogenic autoinflammatory diseases: new insights into clinical aspects and pathogenesis.

Cailin Henderson, Raphaela Goldbach-Mansky

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in rheumatology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

30 citing papers in PubMed, 68 citations in OpenAlex.

  1. Trial
  2. Review
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  7. Review
  8. Article
  9. Article
  10. Review
  11. Autoinflammation and HLA-B27: Beyond Antigen Presentation.Ocular immunology and inflammation · 2016
    Review
  12. Observational
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
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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

2 authors at 1 institution in 1 country.

Cailin HendersonTranslational Autoinflammatory Disease Section, MSC 1560, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Raphaela Goldbach-Mansky
National Institutes of Health · US

Funding

Clinical Support Services for the NIAMS Intramural Research ProgramZIDAR041180 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI COLBERT, ROBERT · 2009 to 2025
$119.2M
Pathogenesis and treatment studies in patients with NOMID and related diseasesZIAAR041138 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI GOLDBACH-MANSKY, RAPHAELA · 2009 to 2016
$8.6M
Pathogenesis and treatment studies in patients with NOMID and related diseasesZ01AR041138 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI GOLDBACH-MANSKY, RAPHAELA · 2003 to 2008
$2.3M
Pathogenesis of Behcet's disease and Still's diseaseZIAAR041194 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI GOLDBACH-MANSKY, RAPHAELA · 2011 to 2013
$1.2M
Intramural NIH HHS Z01 AR041138Intramural NIH HHS ZIA AR041138
6 · The paper itself

Abstract

purpose of reviewThe genetic and clinical characterizations of monogenic autoinflammatory syndromes have led to ground breaking insights into the regulation of inflammatory responses to endogenous and exogenous inducers or triggers of inflammation and continue to uncover key inflammatory pathways of the innate immune system. This article summarizes recent progress in the clinical aspects and understanding of the pathogenesis of this growing spectrum of diseases. RECENT

findingsThe understanding of the spectrum of organ manifestations in autoinflammation was expanded by the discovery of two novel monogenic diseases both caused by the absence of an anti-inflammatory signal and added evidence that increased IL-1 signaling can cause aseptic osteolytic bone lesions and that the absence of IL-10 signaling causes inflammatory enterocolitis in neonates. New knock in animal models for TNF-receptor-associated periodic syndrome, and familial Mediterranean fever and cryopyrin-associated periodic syndromes allow insights into the complexity of the dysregulated immune pathways. Exploring 'triggers' of the NLRP3 inflammasome spurred studies of tissue inflammation in diseases including gout and those that previously have not been considered inflammatory in nature such as diabetes, fibrosing lung disease and possibly coronary artery disease. SUMMARY: The genetic characterization of a growing number of monogenic autoinflammatory diseases has provided important insights into the phenotypic expression of single gene disorders and the complexity of the dysregulated inflammatory pathways leading to clinical disease. Knowledge obtained from these disorders is pertinent to a number of common disorders and provides new targets for drug development.

Indexed as

CytokinesHereditary Autoinflammatory DiseasesHumansCytokines

Identifiers

PMID20671522
PMCPMC3020910
OpenAlexW2028801296

What OpenQuestion holds

Textmetadata
LicenceTDM
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.