Evidence map›Paper›PMID 21632208›Full record

ReviewJournal of autoimmunity2011

Pathogenesis of systemic lupus erythematosus revisited 2011: end organ resistance to damage, autoantibody initiation and diversification, and HLA-DR.

Shu Man Fu, Umesh S Deshmukh, Felicia Gaskin

Abstract readHistorical ArticleReview
In one paragraph

Review in Journal of autoimmunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
8.2field-weighted citation impact, top 2% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

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  16. Methyl salicylate 2-Drug design, development and therapy · 2016
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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

3 authors at 1 institution in 1 country.

Shu Man FuDivision of Clinical Rheumatology, University of Virginia, Charlottesville, VA 22908-0412, USA. sf2e@virginia.edu
Umesh S Deshmukh
Felicia Gaskin
University of Virginia · US

Funding

Cellular and Genetic Basis of Systemic LupusR01AR047988 · NIAMS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI FU, SHU MAN · 2001 to 2020
$8.4M
SPECIALIZED CENTER OF RESEARCH ON SYSTEMIC LUPUS ERYTHEMP50AR045222 · NIAMS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI FU, SHU MAN · 1998 to 2006
$7.9M
HLA-D Region Systemic Lupus Erythematosus PathogenesisR01AR049449 · NIAMS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI FU, SHU MAN · 2005 to 2015
$4.2M
T Cell Epitope Mimicry for Autoimmune Responses in SLER01AI079621 · NIAID · UNIVERSITY OF VIRGINIA · PI DESHMUKH, UMESH S, FU, SHU MAN · 2009 to 2013
$2.2M
Genetics of Autontibody DiversificationK01AR051391 · NIAMS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI DESHMUKH, UMESH S · 2004 to 2008
$499k
NIAID NIH HHS R01 AI079621NIAID NIH HHS R01-AI079621NIAMS NIH HHS K01 AR051391NIAMS NIH HHS KO1 AR051391NIAMS NIH HHS P50-AR04522NIAMS NIH HHS P50 AR045222NIAMS NIH HHS R01 AR047988NIAMS NIH HHS R01-AR047988NIAMS NIH HHS R01 AR049449NIAMS NIH HHS R01-AR049449
6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is a multi-system disorder resulting from interaction of susceptibility genes and environmental factors. SLE has protean clinical presentations at the initial diagnosis and relapses. SLE-related autoantibodies have unique patterns of diversification to linked proteins such as the snRNP particle and the diversification takes years before clinical diagnosis. There are both clinical and experimental evidence to indicate that separate genes contribute to autoimmunity and end organ damage and these genes are independent and interactive. Among the numerous susceptibility genes, HLA-D complex is dominant. Results from the authors' laboratories led us to postulate a unified hypothesis for SLE pathogenesis. This hypothesis states that SLE-autoantibodies are initiated by environmental T cell epitope mimics of the SLE-related autoantigens in hosts with susceptible HLA-D alleles. These autoantibodies diversify over a period of years due the accumulation of cross-reactive T cells. This process ultimately leads to the generation of organ specific autoantibodies and autoreactive effector T cells due to the polyreactive nature of T and B cell receptors from hosts with susceptibility genes to end organ damage, resulting in protean clinical presentations. This hypothesis accounts for most of the features unique to SLE and has clinical implications as to how patients should be treated.

Indexed as

AnimalsAntibody DiversityAutoantibodiesB-LymphocytesGene-Environment InteractionGenetic Predisposition to DiseaseHistory, 20th CenturyHistory, 21st CenturyHLA-DR AntigensHumansLupus Erythematosus, SystemicModels, ImmunologicalMultiple Organ FailureT-LymphocytesAutoantibodiesHLA-DR Antigens

Identifiers

PMID21632208
PMCPMC3173577
OpenAlexW2091122779

What OpenQuestion holds

Textmetadata
LicenceTDM
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.