Evidence map›Paper›PMID 19302045›Full record

ReviewAnnual review of immunology2009

Recent advances in the genetics of autoimmune disease.

Peter K Gregersen, Lina M Olsson

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Annual review of immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
134citing papers in PubMed, 7 pooled it
–field-weighted citation impact
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

134 citing papers in PubMed, 7 syntheses or guidelines pooled it.

  1. Autoimmunity and hernia mesh: fact or fiction?Hernia : the journal of hernias and abdominal wall surgery · 2023
    Pooled it
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  15. Genetic Polymorphism ofMedicina (Kaunas, Lithuania) · 2022
    Review
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  17. Review
  18. Review
  19. Article
  20. Article

74 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

2 authors.

Peter K GregersenRobert S. Boas Center for Genomics and Human Genetics, The Feinstein Institute for Medical Research, Manhasset, New York 11030, USA. peterg@nshs.edu
Lina M Olsson

Funding

WHITE MATTER STRUCTURAL DEFICITS IN HIGH FUNCTIONING CHILDREN WITH AUTISM SPEM01RR018535 · NCRR · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI SCHWARTZ, GUY · 2003 to 2010
$19.5M
NARAC The Genetics of Rheumatoid ArthritisR01AR044422 · NIAMS · NORTH SHORE UNIVERSITY HOSPITAL · PI GREGERSEN, PETER K. · 1997 to 2011
$6.0M
Mapping Autoimmune Phenotypes in Multiplex FamiliesR01AI068759 · NIAID · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI GREGERSEN, PETER K. · 2007 to 2011
$4.7M
GENETICS OF RHEUMATOID ARTHRITIS-264972232N01AR072232 · NIAMS · NORTH SHORE UNIVERSITY HOSPITAL · 1997 to 2003
$818k
SYNTHESIS OF ANTITUMOR CRYPTOPHYCIN A AND ITS MIMICSF32CA072232 · NCI · UNIVERSITY OF PENNSYLVANIA · PI GUISE, LISA E · 1996 to 1997
–
AUTOIMMUNE BIOMARKERS COLLABORATIVE NETWORK-264012256N01AR012256 · NIAMS · NORTH SHORE UNIVERSITY HOSPITA · 2002 to 2003
–
STUDIES ON THE POLYMERIZATION OF SICKLE CELL HEMOGLOBINR01HL012256 · NHLBI · GEORGETOWN UNIVERSITY · PI DE LEVIE, ROBERT · 1985 to 1985
–
NCI NIH HHS N01 AR072232NCRR NIH HHS M01 RR018535NHLBI NIH HHS N01 AR012256NIAID NIH HHS AI068759NIAID NIH HHS R01 AI068759NIAMS NIH HHS AR12256NIAMS NIH HHS AR44422NIAMS NIH HHS AR72232NIAMS NIH HHS N01 AR012256NIAMS NIH HHS R01 AR044422
6 · The paper itself

Abstract

Extraordinary technical advances in the field of human genetics over the past few years have catalyzed an explosion of new information about the genetics of human autoimmunity. In particular, the ability to scan the entire genome for common polymorphisms that associate with disease has led to the identification of numerous new risk genes involved in autoimmune phenotypes. Several themes are emerging. Autoimmune disorders have a complex genetic basis; multiple genes contribute to disease risk, each with generally modest effects independently. In addition, it is now clear that common genes underlie multiple autoimmune disorders. There is also heterogeneity among subphenotypes within a disease and across major racial groups. The current crop of genetic associations are only the start of a complete catalog of genetic factors for autoimmunity, and it remains unclear to what extent common variation versus multiple rare variants contribute to disease susceptibility. The current review focuses on recent discoveries within functionally related groups of genes that provide clues to novel pathways of pathogenesis for human autoimmunity.

Indexed as

Genetic Predisposition to DiseaseAdaptor Proteins, Signal TransducingAnimalsAutoimmune DiseasesAutoimmunityCytokinesGene FrequencyGenome, HumanHumansMembrane ProteinsNF-kappa BProtein Tyrosine Phosphatase, Non-Receptor Type 22Receptors, Pattern RecognitionReceptors, Tumor Necrosis FactorSignal TransductionTranscription FactorsAdaptor Proteins, Signal TransducingBANK1 protein, humanCytokinesMembrane ProteinsNF-kappa BProtein Tyrosine Phosphatase, Non-Receptor Type 22PTPN22 protein, humanReceptors, Pattern RecognitionReceptors, Tumor Necrosis FactorTranscription Factors

Identifiers

PMID19302045
PMCPMC2992886

What OpenQuestion holds

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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.