Evidence map›Paper›PMID 15004750›Full record

ArticleHuman genetics2004

Association between IFNA genotype and the risk of sarcoidosis.

Mitsuteru Akahoshi, Mami Ishihara, Natascha Remus, Kazuko Uno, Katsuhisa Miyake, Tomomitsu Hirota, Kazuko Nakashima, Akira Matsuda, Mizuo Kanda, Tadao Enomoto and 7 more

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Human genetics, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 8% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. The Immunogenetics of Granulomatous Diseases.Advances in experimental medicine and biology · 2022
    Article
  6. Plasmacytoid dendritic cells in cutaneous sarcoidosis.Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2018
    Article
  7. Familial sarcoidosis: Report of a mother and her son.European journal of rheumatology · 2017
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Conversion events in gene clusters.BMC evolutionary biology · 2011
    Article
  14. Article
  15. Review
  16. Tuberculosis as a complex trait: impact of genetic epidemiological study design.Mammalian genome : official journal of the International Mammalian Genome Society · 2011
    Review
  17. Review
  18. Article
  19. Dendritic cells in the pathogenesis of sarcoidosis.American journal of respiratory cell and molecular biology · 2010
    Review
  20. 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

17 authors at 12 institutions in 3 countries.

Mitsuteru AkahoshiLaboratory for Genetics of Allergic Diseases, SNP Research Center, Institute of Physical and Chemical Research, RIKEN Yokohama Institute, Yokohama, Japan.
Mami Ishihara
Natascha Remus
Kazuko Uno
Katsuhisa Miyake
Tomomitsu Hirota
Kazuko Nakashima
Akira Matsuda
Mizuo Kanda
Tadao Enomoto
Shigeaki Ohno
Hitoshi Nakashima
Jean-Laurent Casanova
Julian M Hopkin
Mayumi Tamari
Xiao-Quan Mao
Taro Shirakawa
Hokkaido University · JPKyoto University · JPKyushu University · JPRIKEN · JPRIKEN Center for Integrative Medical Sciences · JPInserm · FRJapanese Red Cross Society Wakayama Medical Center · JPLouis Pasteur Center for Medical Research · JPUniversité Paris Cité · FRUniversity of Wales · GBWakayama Rosai Hospital · JPYokohama City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sarcoidosis is known to be a systemic granulomatous disorder characterized by a cell-mediated Th1-type inflammatory response. To identify a key genetic factor in the pathogenesis of sarcoidosis, we investigated single nucleotide polymorphisms within 10 candidate genes involved in type 1 immune process ( IFNA17, IFNB, IFNG, IFNGR1, IFNGR2, IL12B, IL12RB1, IL12RB2, ETA-1, and NRAMP1) in an association-based study of 102 Japanese patients with sarcoidosis, 114 with tuberculosis, and 110 control subjects. After correction for multiple testing, an IFNA17 polymorphism (551T-->G) was found to be associated with susceptibility to sarcoidosis (odds ratio 3.27 [95% CI: 1.44-7.46], P=0.004, P(c)=0.04), but not to tuberculosis. We observed no significant associations with the other polymorphisms of the Th1-related genes. We further typed another IFNA polymorphism ( IFNA10 60T-->A) and confirmed two major haplotypes of the IFNA gene, viz., allele 1: IFNA10 [60T]- IFNA17 [551T] and allele 2: IFNA10 [60A]- IFNA17 [551G], in the Japanese population. In healthy subjects, IFNA allele 2, which is over-represented in patients with sarcoidosis, was significantly associated with increased IFN-alpha and IL-12p70 production induced by Sendai virus in vitro. This study suggests that possession of the IFNA allele with higher levels of IFN-alpha significantly increases the risk of sarcoidosis.

Indexed as

Risk FactorsAdolescentAdultAgedBiological AssayCase-Control StudiesChildDNA PrimersEnzyme-Linked Immunosorbent AssayFemaleGene FrequencyHaplotypesHumansInterferon-alphaInterferonsInterleukin-12DNA PrimersIFNA17 protein, humanInterferon-alphaInterferonsInterleukin-12

Identifiers

PMID15004750
OpenAlexW1984036704

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.