ReviewPediatric rheumatology online journal2025
Update on new autoinflammatory disorders from the 2024 Pediatric Rheumatology European Society Congress.
Review in Pediatric rheumatology online journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- Mechanisms outpacing medicine in autoinflammatory diseases.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Since the molecular characterization of periodic fever syndromes led to the concept of autoinflammation, the pace of scientific advancement in this field has been dramatic. Here, we review many of the most impactful new discoveries in autoinflammation, as presented at the 2024 Pediatric Rheumatology European Society Congress. This includes new genes and diseases, such as SHARPIN mutations and dominant-negative mutations in OTULIN as causes of disorders of ubiquitination, PMVK mutations as potential causes of a mevalonate kinase deficiency mimic, and ARF1 and REXO2 as causes of interferonopathy. Several new molecular mechanisms and mutations were also reported for older diseases including coatomer protein complex subunit alpha (COPA) syndrome, Aicardi-Goutières syndrome, PLCG2-associated immune dysregulation (PLAID), and NLRP3-AID. Finally, molecular and omics studies of STING1-associated vasculopathy with onset in infancy (SAVI) and haploinsufficiency of A20 (HA20) contributed to advances in underlying autoinflammatory biology.
Indexed as
Identifiers
What Socratic holds
Registered trials
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.