Evidence mapPaperPMID 32044247Full record

ReviewBest practice & research. Clinical rheumatology2020

The microbiome in autoimmune rheumatic disease.

Maximilian F Konig

Open access · greenAbstract readReview
In one paragraph

Review in Best practice & research. Clinical rheumatology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 2 pooled it
9.7field-weighted citation impact, top 1% 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

52 citing papers in PubMed, 2 syntheses or guidelines pooled it, 86 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Review
  6. Mucosal-Associated Invariant T Cells in Rheumatic Diseases.Arthritis & rheumatology (Hoboken, N.J.) · 2026
    Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Vitiligo: are microbes to blame?Bioscience of microbiota, food and health · 2025
    Review
  14. Head to head comparison ofClinical rheumatology · 2024
    Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. 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

1 author at 1 institution in 1 country.

Maximilian F KonigDivision of Rheumatology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA. Electronic address: konig@jhmi.edu.
Johns Hopkins Medicine · US

Funding

Multidisciplinary Rheumatology Training ProgramT32AR048522 · JOHNS HOPKINS UNIVERSITY · 2003 to 2025
$766k
NIAMS NIH HHS T32 AR048522
6 · The paper itself

Abstract

Microbial contributions to the immunopathogenesis of autoimmune rheumatic diseases have been studied since the advent of germ theory in the 19th century. With the exception of Group A Streptococcus in rheumatic fever, early studies failed to establish causal relationships between specific pathobionts and rheumatic disease. Today, systemic autoimmune diseases are thought to result from a complex interplay of environmental factors, individual genetic risk, and stochastic events. Interactions of microbiota and the immune system have been shown to promote and sustain chronic inflammation and autoimmunity. In mechanistic studies, microbe-immune cell interactions have been implicated in the initiation of autoimmune rheumatic diseases, e.g., through the posttranslational modification of autoantigens in rheumatoid arthritis or through neutrophil cell death and cross-reactivity with commensal orthologs in systemic lupus erythematosus. In parallel, modern molecular techniques have catalyzed the study of the microbiome in systemic autoimmune diseases. Here, I review current insights gained into the skin, oral, gut, lung, and vascular microbiome in connective tissue diseases and vasculitis. Mechanism relevant to the development and propagation of autoimmunity will be discussed whenever explored. While studies on autoimmune rheumatic disease have almost invariably shown abnormal microbiome structure (dysbiosis), substantial variability in microbial composition between studies makes generalization difficult. Moreover, an etiopathogenic role of specific pathobionts cannot be inferred by association alone. Integrating descriptive studies of microbial communities with hypothesis-driven research informed by immunopathogenesis will be important in elucidating targetable mechanisms in preclinical and established rheumatic disease.

Indexed as

Autoimmune DiseasesLupus Erythematosus, SystemicMicrobiotaRheumatic DiseasesAutoimmunityDysbiosisHumansConnective tissue diseaseMicrobiomePathobiontsRheumatoid arthritisSclerodermaSjögren's syndromeSystemic sclerosisVasculitis

Identifiers

PMID32044247
PMCPMC7295668
OpenAlexW3005523241

What Socratic 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 Socratic graph.