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Background Interleukin 13 (IL-13) and IL-4 are archetypal cytokines that drive type 2 immune responses, which are dysregulated in a large proportion of patients with asthma. The regulation of IL-13 and IL-4 signalling has focused on their downstream events (e.g. phosphorylation of STAT6 upon receptor binding) leading to transcription of type 2 mediators. Further regulators of this fundamental pathway remain poorly understood. Likewise, molecular markers of type 2 disease remain scarce.Methods We used RNA immunoprecipitation, siRNA and shRNA depletion in cell lines and primary bronchial epithelium, as well as RT-qPCR and protein analyses (western blotting, MSD). We also employed Frac-seq (subcellular fractionation and RNA-sequencing) to compare steady (transcription) vs polyribosome-bound (translation) mRNA expression in response to IL-13 in an IGF2BP3-dependent manner. We explored several datasets of ‘type 2 high’ disease cohorts.Results Using RNA immunoprecipitation, we detected IGF2BP3 directly bound to the mRNAs encoding for IL4R and IL13Ra1. Depletion of IGF2BP3 led to an increase of IL-4Ra and IL-13Ra1 cell surface expression, without affecting IL4R or IL13RA1 mRNA levels, methylation or stability in human bronchial epithelial BEAS-2B cells. Concomitantly, IGF2BP3 depletion led to increased IL-13-dependent STAT6 phosphorylation and activity as determined by a STAT6-reporter and increased expression of IL-13-dependent eotaxins CCL26, CCL24 and CCL11 mRNAs, as well as the classically associated Th2 marker GATA3. IGF2BP3 regulation of eotaxin and GATA3 expression was recapitulated in primary airway cells. Frac-seq demonstrated that IL-13 triggers different transcriptional and post-transcriptional responses, with IGF2BP3 levels mainly modulating steady mRNA levels. We also found IGF2BP3 upregulated in multiple cohorts of atopic and type 2 high asthmatic patients.Conclusions We show for the first time that an RNA binding protein modulates IL-13/IL-4 signalling and offer a novel approach for suppressing IL-13-dependent signalling in bronchial epithelium. IGF2BP3 is increased in type 2 high disease, where it may be part of a feedback loop to halt type 2 inflammation and serve as a novel biomarker.