ArticleFrontiers in immunology2026
Free Epstein-Barr virus-induced gene 3 functions as an autonomous immunosuppressive cytokine to maintain immune tolerance.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Epstein-Barr virus-induced gene 3(EBI3) is conventionally viewed as a subunit of IL-27 and IL-35, yet the function of uncomplexed "free" EBI3 is unknown. We show that free EBI3 is an autonomous immunosuppressive cytokine that acts via a gp130/WSX-1/STAT3 axis and epigenetic reprogramming. A free-EBI3-specific sandwich ELISA revealed 23.3 ± 2.2 ng/mL in healthy human sera and equivalent levels in mice; no cross-reactivity with IL-27/IL-35 was observed. Serum free EBI3 was reduced in rheumatoid arthritis(RA; 12.4 ± 1.4 ng/mL) and multiple sclerosis (MS; 14.6 ± 1.4 ng/mL; both p< 0.001) and inversely correlated with disease activity(RA-DAS28-ESR r=-0.67; MS-EDSS r=-0.61). Baseline<15 ng/mL predicted higher flare risk(RA HR = 2.8;MS HR = 3.2;p<0.01). Recombinant free EBI3 activated STAT3 exclusively(EC50≈16 nM), suppressed T-cell proliferation (-40%),IFN-y(-45%) and IL-17(-60%),and drove M2 macrophage polarization (+2.7-fold;p<0.001).Epigenetically,it reduced H3K4me3 at Ifng/Il4 promoters, induced Il10/Tgfb hypomethylation(-35%/-28%), and remodeled 1,021 chromatin-accessible STAT3/NF-kB sites. EBI3
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