ArticleFrontiers in immunology2025
IRAK3 is upregulated in rheumatoid arthritis synovium and delays the onset of experimental arthritis.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Stigmasterol ameliorates Freund's complete adjuvant-induced polyarthritis in rats.Inflammopharmacology · 2026Article
- Interleukin-1 Receptor-Associated Kinase 3 Attenuates Chondrocyte Senescence and Osteoarthritis via Inhibition of the TLR7/9-NF-κB Axis.Journal of molecular histology · 2026Article
- Inhibiting METTL3 in macrophages alleviates colitis by enhancing M2 polarization via upregulating IRAKM.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
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Authors and funding
3 authors.
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Abstract
Tumour necrosis factor (TNF) is a potent inducer of endotoxin tolerance-associated molecules, such as interleukin-1 receptor-associated kinase 3 (IRAK3), and also a therapeutic target in inflammatory autoimmune diseases, as it upregulates the production of inflammatory mediators. The role of IRAK3 was assessed in rheumatoid arthritis (RA), a disease which is amenable to TNF blockade. As a variant of IRAK3 lacks the death domain required for its canonical role, isoform expression was determined in different inflammatory milieu by immunoblotting. RA synovial explant expression of IRAK3 was measured by qPCR. The expression of the larger, "classical" IRAK3 isoform predominated in macrophages treated with various stimuli. The expression of IRAK3 was higher in RA synovium compared to osteoarthritis synovium. Using collagen-induced arthritis, a murine model of RA, the immunomodulatory role of IRAK3 was investigated with wild-type (WT) and IRAK3-deficient mice expressing the MHC-II A
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