Evidence map›Paper›PMID 25419237›Full record

ArticleGenome medicine2014

Expression profiles of long non-coding RNAs located in autoimmune disease-associated regions reveal immune cell-type specificity.

Barbara Hrdlickova, Vinod Kumar, Kartiek Kanduri, Daria V Zhernakova, Subhash Tripathi, Juha Karjalainen, Riikka J Lund, Yang Li, Ubaid Ullah, Rutger Modderman and 6 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Genome medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
4.4field-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

67 citing papers in PubMed, 107 citations in OpenAlex.

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  12. Single-cell RNA sequencing uncovers the nuclear decoy lincRNA PIRAT as a regulator of systemic monocyte immunity during COVID-19.Proceedings of the National Academy of Sciences of the United States of America · 2022
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  13. Celiac disease: From genetics to epigenetics.World journal of gastroenterology · 2022
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7 more citing papers are in PubMed but not listed here.

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

16 authors at 5 institutions in 2 countries.

Barbara HrdlickovaDepartment of Genetics, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Vinod KumarDepartment of Genetics, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Kartiek KanduriTurku Center for Biotechnology, University of Turku, and Åbo Akademi University, Turku, Finland.
Daria V ZhernakovaDepartment of Genetics, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Subhash TripathiTurku Center for Biotechnology, University of Turku, and Åbo Akademi University, Turku, Finland.
Juha KarjalainenDepartment of Genetics, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Riikka J LundTurku Center for Biotechnology, University of Turku, and Åbo Akademi University, Turku, Finland.
Yang LiDepartment of Genetics, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Ubaid UllahTurku Center for Biotechnology, University of Turku, and Åbo Akademi University, Turku, Finland.
Rutger ModdermanDepartment of Genetics, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Wayel AbdulahadDepartment of Rheumatology and Clinical Immunology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Harri LähdesmäkiTurku Center for Biotechnology, University of Turku, and Åbo Akademi University, Turku, Finland ; Department of Information and Computer Science, Aalto University, Espoo, Finland.
Lude FrankeDepartment of Genetics, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Riitta LahesmaaTurku Center for Biotechnology, University of Turku, and Åbo Akademi University, Turku, Finland.
Cisca WijmengaDepartment of Genetics, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Sebo WithoffDepartment of Genetics, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
University Medical Center Groningen · NLUniversity of Turku · FIUniversity of Groningen · NLAalto University · FIÅbo Akademi University · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlthough genome-wide association studies (GWAS) have identified hundreds of variants associated with a risk for autoimmune and immune-related disorders (AID), our understanding of the disease mechanisms is still limited. In particular, more than 90% of the risk variants lie in non-coding regions, and almost 10% of these map to long non-coding RNA transcripts (lncRNAs). lncRNAs are known to show more cell-type specificity than protein-coding genes.

methodsWe aimed to characterize lncRNAs and protein-coding genes located in loci associated with nine AIDs which have been well-defined by Immunochip analysis and by transcriptome analysis across seven populations of peripheral blood leukocytes (granulocytes, monocytes, natural killer (NK) cells, B cells, memory T cells, naive CD4(+) and naive CD8(+) T cells) and four populations of cord blood-derived T-helper cells (precursor, primary, and polarized (Th1, Th2) T-helper cells).

resultsWe show that lncRNAs mapping to loci shared between AID are significantly enriched in immune cell types compared to lncRNAs from the whole genome (α <0.005). We were not able to prioritize single cell types relevant for specific diseases, but we observed five different cell types enriched (α <0.005) in five AID (NK cells for inflammatory bowel disease, juvenile idiopathic arthritis, primary biliary cirrhosis, and psoriasis; memory T and CD8(+) T cells in juvenile idiopathic arthritis, primary biliary cirrhosis, psoriasis, and rheumatoid arthritis; Th0 and Th2 cells for inflammatory bowel disease, juvenile idiopathic arthritis, primary biliary cirrhosis, psoriasis, and rheumatoid arthritis). Furthermore, we show that co-expression analyses of lncRNAs and protein-coding genes can predict the signaling pathways in which these AID-associated lncRNAs are involved.

conclusionsThe observed enrichment of lncRNA transcripts in AID loci implies lncRNAs play an important role in AID etiology and suggests that lncRNA genes should be studied in more detail to interpret GWAS findings correctly. The co-expression results strongly support a model in which the lncRNA and protein-coding genes function together in the same pathways.

Identifiers

PMID25419237
PMCPMC4240855
OpenAlexW2119828270

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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.