Evidence map›Paper›PMID 18273033›Full record

ArticleGenes and immunity2008

Association of LILRA2 (ILT1, LIR7) splice site polymorphism with systemic lupus erythematosus and microscopic polyangiitis.

K Mamegano, K Kuroki, R Miyashita, M Kusaoi, S Kobayashi, K Matsuta, K Maenaka, M Colonna, S Ozaki, H Hashimoto and 3 more

Erratum issuedAbstract readComparative Study
PubMed Publisher
In one paragraph

Article in Genes and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.3field-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

21 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
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  3. Get Spliced: Uniting Alternative Splicing and Arthritis.International journal of molecular sciences · 2024
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  10. Review
  11. The Genomic Organization of theFrontiers in immunology · 2021
    Review
  12. Review
  13. Review
  14. Review
  15. Genetics of ANCA-associated Vasculitides.Current rheumatology reports · 2014
    Review
  16. Review
  17. Article
  18. Leukocyte immunoglobulin-like receptors as new players in autoimmunity.Clinical reviews in allergy & immunology · 2010
    Review
  19. Review
  20. Review
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

13 authors at 6 institutions in 2 countries.

K MameganoDepartment of Human Genetics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
K Kuroki
R Miyashita
M Kusaoi
S Kobayashi
K Matsuta
K Maenaka
M Colonna
S Ozaki
H Hashimoto
Y Takasaki
K Tokunaga
N Tsuchiya
Juntendo University · JPThe University of Tokyo · JPKyushu University · JPSt. Marianna University School of Medicine · JPUniversity of Tsukuba · JPWashington University in St. Louis · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Leukocyte immunoglobulin-like receptors (LILRs) are inhibitory, stimulatory or soluble receptors encoded within the leukocyte receptor complex. Some LILRs are extensively polymorphic, and exhibit evidence for balancing selection and association with disease susceptibility. LILRA2 (LIR7/ILT1) is an activating receptor highly expressed in inflammatory tissues, and is involved in granulocyte and macrophage activation. In this study, we examined the association of LILRA2 and adjacently located LILRA1 with systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) and microscopic polyangiitis (MPA). Polymorphism screening detected a LILRA2 SNP (rs2241524 G>A) that disrupts splice acceptor site of intron 6. Case-control association studies on 273 Japanese SLE, 296 RA, 50 MPA and 284 healthy individuals revealed increase of genotype A/A in SLE (12.1%, odds ratio (OR) 1.82, 95% confidence interval (CI) 1.02-3.24, P=0.041) and in MPA (16.0%, OR 2.52, 95% CI 1.07-5.96, P=0.049) compared with healthy individuals (7.0%). The risk allele caused an activation of a cryptic splice acceptor site that would lead to a novel LILRA2 isoform lacking three amino acids in the linker region (Delta 419-421). Flow cytometry indicated that this isoform was expressed on the surface of monocytes. These findings suggested that LILRA2 Delta 419-421 isoform encoded by the splice site SNP may play a role in SLE and MPA.

Indexed as

Alternative SplicingAsian PeopleBase SequenceDNA PrimersFlow CytometryGenetic Predisposition to DiseaseGenotypeHumansLupus Erythematosus, SystemicMolecular Sequence DataMonocytesOdds RatioPolymorphism, Single NucleotideReceptors, ImmunologicReverse Transcriptase Polymerase Chain ReactionSequence Analysis, DNADNA PrimersLILRA2 protein, humanReceptors, Immunologic

Identifiers

PMID18273033
OpenAlexW1981815125

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.