ArticleArthritis research & therapy2026
Differential regulation of SOCS signalling and immunoproteasome pathways by JAK inhibitors and TNF inhibitors in rheumatoid arthritis.
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
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundJanus kinase (JAK) inhibitors and TNF inhibitors (TNFi) are established therapies in rheumatoid arthritis (RA), yet their differential effects on the JAK/STAT/SOCS/proteasome axis remain incompletely understood. This pilot study systematically characterised treatment-specific effects of baricitinib, tofacitinib, and TNFi upon molecular signatures in RA patients.
methodsSeventy-five patients with RA were enrolled across two prospective cohorts: an initial inception cohort treated with tofacitinib (n = 15) and a subsequent confirmatory cohort treated with baricitinib or TNFi (n = 60; baricitinib n = 29, TNFi n = 31), along with 17 and 33 healthy donors (HD)serving as controls for each cohort, respectively. mRNA expression of SOCS1, SOCS2, SOCS3, CIS1, and the immunoproteasome subunit β2i was assessed in peripheral blood mononuclear cells by real-time PCR. SOCS2 protein levels were measured by ELISA, and serum IL-6 levels were evaluated in the baricitinib/TNFi cohort.
resultsResponder rates were comparable across all three treatment groups at both time points. JAK inhibition was associated with a distinct SOCS suppression signature: SOCS2 mRNA declined progressively under both baricitinib and tofacitinib but not under TNFi blockade. SOCS1 and SOCS3 mRNA normalized under baricitinib over time, while SOCS3 elevation persisted throughout the observation period under TNFi. CIS1 was selectively suppressed under baricitinib. Partial discordance between SOCS2 mRNA and protein levels suggested post-transcriptional regulation. Baseline SOCS3 expression was significantly higher in baricitinib non-responders than responders, and early SOCS3 decline at 2 weeks distinguished TNFi responders from non-responders. Proteasomal β2i mRNA was relatively upregulated under tofacitinib and TNFi but not under baricitinib.
conclusionJAK inhibition drives a treatment-specific suppression of SOCS family members not observed under TNFi, reflecting differential remodelling of cytokine feedback networks. Baseline and early SOCS3 dynamics emerge as candidate biomarkers of treatment response. These findings may inform future efforts to personalise treatment selection in RA and warrant validation in larger, randomised cohorts.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.