Evidence map›Paper›PMID 31197599›Full record

ReviewCurrent rheumatology reports2019

ILC3 in Axial Spondyloarthritis: the Gut Angle.

Daniele Mauro, Federica Macaluso, Serena Fasano, Riccardo Alessandro, Francesco Ciccia

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current rheumatology reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

22 citing papers in PubMed, 37 citations in OpenAlex.

  1. Exhaustion-Resistant CD8Immunology · 2025
    Review
  2. Review
  3. T-betHeliyon · 2025
    Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. The bone marrow side of axial spondyloarthritis.Nature reviews. Rheumatology · 2023
    Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. The gut-joint axis in rheumatoid arthritis.Nature reviews. Rheumatology · 2021
    Review
  18. Review
  19. Article
  20. Innate lymphoid cells in inflammatory arthritis.Arthritis research & therapy · 2020
    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

5 authors at 2 institutions in 1 country.

Daniele MauroDipartimento di Medicina di Precisione, Section of Rheumatology, Università degli Studi della Campania "Luigi Vanvitelli", Naples, Italy.
Federica MacalusoDipartimento di Medicina di Precisione, Section of Rheumatology, Università degli Studi della Campania "Luigi Vanvitelli", Naples, Italy.
Serena FasanoDipartimento di Medicina di Precisione, Section of Rheumatology, Università degli Studi della Campania "Luigi Vanvitelli", Naples, Italy.
Riccardo AlessandroDipartimento di Biopatologia e Biotecnologie Mediche, Università di Palermo, Palermo, Italy.
Francesco CicciaDipartimento di Medicina di Precisione, Section of Rheumatology, Università degli Studi della Campania "Luigi Vanvitelli", Naples, Italy. francesco.ciccia@unicampania.it.
University of Palermo · ITUniversity of Campania "Luigi Vanvitelli" · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewA growing body of evidence supports the relevance of the interleukin-23/interleukin-17 (IL-23/IL-17) pathway for the pathogenesis of axial spondyloarthritis (axSpA) and its treatment. Recently, innate lymphoid cells (ILC), a heterogeneous family of immune effector cells, have been identified as a relevant contributor in tissue homeostasis, partially via IL-23/IL-17 axis. This review describes the biology and the origins of the group 3 ILCs (ILC3s) in humans, focusing on their role in the pathogenesis of axSpA. RECENT

findingsClinical trials showed the effectiveness of IL23/IL-17 axis inhibition in both spondyloarthritis (SpA) and Inflammatory Bowel Disease (IBD). Recent findings confirm the high prevalence of subclinical gut inflammation in patients with SpA. Translational data in humans have demonstrated an increase in the number of ILC3s responsive to IL-23 and producing either IL-22 or IL-17 in the gut of SpA patients. The observation of gut-derived ILC3s in circulation and at inflamed tissues in patients with SpA suggest a recirculation of ILCs from mucosal site to lymphoid tissues and possibly enthesis and joints. Multiple observations demonstrate the expansion of IL-17- and IL-22-producing ILC3 in the subclinically inflamed gut of SpA patients. These innate immune cells, also observed in normal entheses, seem to be able to re-circulate from the gut to inflamed tissues of SpA patients, thus contributing to the disease perpetuation. The development of tools that can provide access to diseased tissue from sacroiliac joint and spinal entheses will provide valuable knowledge on the role of ILC3 in axSpA pathogenesis.

Indexed as

HumansImmunity, InnateInflammationInterleukin-17Interleukin-23LymphocytesSpondylarthritisInterleukin-17Interleukin-23Ankylosing spondylitisGroup 3 innate lymphoid cellsGut inflammationIL-17IL-23/IL-17 axisLymphoid tissue inducer cellsSpondyloarthritis

Identifiers

PMID31197599
OpenAlexW2949861824

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.