Evidence map›Paper›PMID 28827978›Full record

ArticlePharmaceutical medicine2017

Defining biological subsets in systemic lupus erythematosus: progress toward personalized therapy.

Nailú Angélica Sinicato, Mariana Postal, Simone Appenzeller, Timothy B Niewold

Abstract read
In one paragraph

Article in Pharmaceutical medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–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

9 citing papers in PubMed.

  1. Trial
  2. Review
  3. Towards precision medicine for systemic lupus erythematosus and neuropsychiatric manifestations.Expert review of precision medicine and drug development · 2025
    Article
  4. Article
  5. Type I interferon antagonists in clinical development for lupus.Expert opinion on investigational drugs · 2020
    Review
  6. Observational
  7. Lessons from precision medicine in rheumatology.Multiple sclerosis (Houndmills, Basingstoke, England) · 2020
    Review
  8. Article
  9. New Trials in Lupus and where Are we Going.Current rheumatology reports · 2018
    Review
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

4 authors.

Nailú Angélica SinicatoRheumatology Unit, Department of Medicine, Faculty of Medical Science, State University of Campinas, Campinas, Brazil.
Mariana PostalRheumatology Unit, Department of Medicine, Faculty of Medical Science, State University of Campinas, Campinas, Brazil.
Simone AppenzellerRheumatology Unit, Department of Medicine, Faculty of Medical Science, State University of Campinas, Campinas, Brazil.
Timothy B NiewoldMayo Clinic, Division of Rheumatology, Department of Immunology, Rochester, MN, USA.

Funding

Interferon Regulatory Factor 5 in Human Lupus PathogenesisR01AR065964 · NIAMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI NIEWOLD, TIMOTHY B · 2015 to 2018
$2.0M
Interferon Alpha as a Tool for Gene Discovery in Human LupusR01AR060861 · NIAMS · UNIVERSITY OF CHICAGO · PI NIEWOLD, TIMOTHY B · 2011 to 2015
$1.8M
The Role of IL-17 Axis in Inflammatory MyositisR01AR057781 · NIAMS · MAYO CLINIC ROCHESTER · PI NIEWOLD, TIMOTHY B, PETERSON, ERIK J · 2010 to 2014
$1.6M
NIAID NIH HHS L30 AI071651NIAMS NIH HHS R01 AR057781NIAMS NIH HHS R01 AR060861NIAMS NIH HHS R01 AR065964
6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is a heterogeneous disease with respect to disease severity, response to treatment, and organ damage. The pathogenesis of SLE includes immunological mechanisms which are driven by both genetic and environmental factors. There are clear differences in the pathogenesis of SLE between patients of different ancestral backgrounds, including differences in genetic risk factors, immunological parameters, and clinical manifestations. Patients with high vs. low levels of type I interferon (IFN) in circulation represents one major biological subset within SLE, and these two groups of patients are present in all ancestral backgrounds. Genetic factors, autoantibodies, and levels of other cytokines all differ between high and low IFN patients. This distinction has also been important in predicting response to treatment with anti-type I IFN therapies, providing a precedent in SLE for biological subsets predicting treatment response. This review will highlight some recent developments in defining biological subsets of SLE based on disease pathophysiology, and the idea that improved knowledge of disease heterogeneity will inform our efforts to personalize therapy in this disease.

Identifiers

PMID28827978
PMCPMC5562038

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.