Evidence map›Paper›PMID 28202919›Full record

ReviewNature reviews. Rheumatology2017

Ectopic lymphoid neogenesis in rheumatic autoimmune diseases.

Michele Bombardieri, Myles Lewis, Costantino Pitzalis

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Rheumatology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 141 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
141citing papers in PubMed, 6 pooled it
12.6field-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

141 citing papers in PubMed, 6 syntheses or guidelines pooled it, 228 citations in OpenAlex.

  1. Pooled it
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  10. Mature tertiary lymphoid structures in pilonidal sinus disease.JID innovations : skin science from molecules to population health · 2026
    Article
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  20. Proceedings of the 2Mediterranean journal of rheumatology · 2026
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81 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

3 authors at 2 institutions in 1 country.

Michele BombardieriCentre for Experimental Medicine and Rheumatology, John Vane Science Centre, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK.
Myles LewisCentre for Experimental Medicine and Rheumatology, John Vane Science Centre, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK.
Costantino PitzalisCentre for Experimental Medicine and Rheumatology, John Vane Science Centre, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK.
Queen Mary University of London · GBWilliam Harvey Research Institute · GB

Funding

Department of Health 11/100/76Medical Research Council G0800648Medical Research Council MR/K015346/1Medical Research Council MR/K020250/1Medical Research Council MR/N003063/1
6 · The paper itself

Abstract

Ectopic lymphoid neogenesis often occurs in the target tissues of patients with chronic rheumatic autoimmune diseases such as rheumatoid arthritis, Sjögren syndrome and other connective tissue disorders, including systemic lupus erythematosus and myositis. However, the mechanisms of ectopic lymphoid-like structure (ELS) formation and function are not entirely understood. For example, it is unclear whether ELSs indicate distinct disease phenotypes or whether they are evolutionary manifestations of chronic inflammation. Also unclear is why ELSs form in some patients but not in others. Nonetheless, ELSs frequently display functional features of ectopic germinal centres and can actively contribute to the maintenance of autoimmunity through the production of disease-specific autoantibodies; furthermore, they seem to influence disease severity and response to both synthetic and biologic DMARDs. In this Review, we discuss current knowledge and gaps in understanding of ELS formation and function including their prevalence in the above rheumatic autoimmune diseases; the mechanisms underlying their formation, maintenance and function, including positive and negative regulatory pathways; their functional relevance in the perpetuation of autoimmunity; their relationship with disease phenotypes, clinical outcomes and response to treatment; and the potential for specific targeting of ELSs through novel therapeutic modalities.

Indexed as

Arthritis, RheumatoidAutoimmune DiseasesHumansLupus Erythematosus, SystemicPrevalenceRheumatic DiseasesSjogren's SyndromeTertiary Lymphoid Structures

Identifiers

PMID28202919
OpenAlexW2588220847

What OpenQuestion holds

Textmetadata
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.