ArticleArthritis research & therapy2026
Soluble factors released from fibroblast-like synoviocytes of JIA patients with future extended course can condition persistent JIA synovial fibroblasts for increased IL-6 production.
Article in Arthritis research & therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
backgroundJuvenile Idiopathic Arthritis (JIA) includes a subset of oligoarticular patients who later extend to a polyarticular course (extended-to-be, ETB), resulting in worse outcomes. Predictors of extension remain poorly defined. We investigated whether interleukin-6 (IL-6) and fibroblast-like synoviocytes (FLS) contribute to this progression.
methodsSynovial fluid samples from persistent oligoarticular patients who remained persistent (≤ 4 joints involved) throughout their disease course and ETB patients were analyzed using protein antibody arrays and ELISA. Importantly, ETB samples were collected prior to clinical extension, and persistent samples were from patients who never extended during the course of their disease. FLS were isolated from synovial fluid and cultured to assess IL-6 secretion. Conditioned media experiments were performed to evaluate whether factors secreted by ETB FLS could influence IL-6 expression in persistent FLS.
resultsMANOVA revealed that (Wilks’ λ = 0.5446, F(9, 31) = 2.88, p = 0.0136) IL-6 and multiple IL-6–related cytokines were significantly elevated in synovial fluid from ETB patients compared to persistent patients. Quantitative ELISA confirmed higher IL-6 concentrations in ETB samples (1.46-fold increase, p = 0.047). FLS isolated from ETB patients prior to extension secreted significantly more IL-6 than persistent FLS (1.6-fold increase, p = 0.0239). Conditioned media from ETB FLS induced IL-6 production in persistent FLS to levels comparable to ETB FLS, demonstrating that soluble factors secreted early by ETB FLS can reprogram persistent FLS toward an inflammatory phenotype, even though these persistent FLS came from patients who remained clinically persistent throughout their disease course.
conclusionsOur findings suggest factors secreted by ETB FLS including IL-6 protein may contribute to disease extension. These data highlight the potential role of early synovial signaling in shaping disease trajectory and support further investigation into IL-6 and FLS as possible therapeutic targets to prevent progression.
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.