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- W2346226980 abstract "Abstract A natural splice variant of IL-4 mRNA omits exon 2. It is unknown whether a corresponding protein, IL-4δ2, is also naturally produced. We have developed an mAb against IL-4δ2 with no cross-reactivity against IL-4. Freshly purified T cells from 8 patients with mild or moderate asthma and from 4 healthy controls were tested after up to 96 h activation with PMA/ionomycin. Levels of IL-4 and IL-4δ2 mRNAs were measured by RT-Q-PCR, and secretion of IL-4 and IL-4δ2 proteins was measured by ELISA. All cells expressed IL-4 and IL-4δ2 mRNAs; stimulation caused a 5-12 fold increase in IL-4 mRNA, and a 20-70 fold increase in IL-4δ2 mRNA at 12-24 h of activation. T cells from controls secreted IL-4 but not IL-4δ2 protein, whereas T cells from asthmatics produced both IL-4 and IL-4δ2 proteins in comparable amounts. Levels of IL-4 protein peaked at 24-48 h of activation, whereas IL-4δ2 protein peaked at 72 h. Adenoviral gene delivery of either mouse IL-4 or mouse IL-4δ2 to mouse lungs in vivo induced immune inflammation with accumulation of T and B cells in both cases. Delivery of IL-4 but not IL-4δ2 induced pulmonary eosinophilia, suggesting that IL-4 does and IL-4δ2 does not engage STAT6 signaling. Experiments in primary human T cell cultures revealed that, indeed, IL-4 but not IL-4δ2 induces phosphorylation of STAT6 or STAT3 in a time- and dose-dependent fashion. Thus, IL-4δ2 is naturally secreted as a protein; it is biologically active in vivo without engaging STAT6 or STAT3 signaling." @default.
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- W2346226980 date "2011-04-01" @default.
- W2346226980 modified "2023-10-16" @default.
- W2346226980 title "Alternatively spliced Interleukin-4 protein is naturally produced in asthmatics, and elicits immune inflammation through a STAT6- and STAT3-independent mechanism (117.14)" @default.
- W2346226980 doi "https://doi.org/10.4049/jimmunol.186.supp.117.14" @default.
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