ReviewCurrent opinion in immunology2012
Coordinating GWAS results with gene expression in a systems immunologic paradigm in autoimmunity.
Review in Current opinion in immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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.
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.
Who cites it
9 citing papers in PubMed.
- Mapping the genetic-transcriptional landscape of thyroid irAEs in sintilimab therapy: toward biomarker-guided immunotoxicity prediction.Frontiers in immunology · 2025Article
- Potential Pathways Associated With Exaggerated T Follicular Helper Response in Human Autoimmune Diseases.Frontiers in immunology · 2018Review
- Follicular Helper T Cells in Systemic Lupus Erythematosus.Frontiers in immunology · 2018Review
- Exploring regulation in tissues with eQTL networks.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Pathophysiology of T follicular helper cells in humans and mice.Nature immunology · 2015Review
- Cellular dissection of psoriasis for transcriptome analyses and the post-GWAS era.BMC medical genomics · 2014Article
- Interindividual variation in human T regulatory cells.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- An inflection point in gene discovery efforts for neurodegenerative diseases: from syndromic diagnoses toward endophenotypes and the epigenome.JAMA neurology · 2013Review
- The dendritic cell response to classic, emerging, and homeostatic danger signals. Implications for autoimmunity.Frontiers in immunology · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
There has been considerable progress in our understanding of the genetic architecture of susceptibility to inflammatory diseases in recent years: several hundred susceptibility loci have been discovered in genome-wide association studies (GWAS) of human populations. This success has created an important challenge in identifying the functional consequences of these risk-associated variants and in elucidating how the repercussions of individual susceptibility loci integrate to yield dysregulation of immune pathways and, ultimately, syndromic clinical phenotypes. The integration of GWAS association signals with high-resolution transcriptome and other genomic data that capture the dynamics of cellular state and function in the context of individual's collection of susceptibility alleles has proven to be a successful avenue of investigation. The rapid pace of methodological development in this area has been coupled with an accumulation of experimental data that makes the elucidation of complex biological networks underlying susceptibility to these common inflammatory diseases a reasonable goal in the near future.
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What OpenQuestion holds
Registered trials
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.