In conclusion, we found that intranasal administration of miR‑410 effectively inhibited airway inflammation in OVA‑induced asthmatic mice by targeting IL‑4 and IL‑13 at the post‑transcriptional level. miR‑410 is thus a promising treatment for allergic asthma.
Therefore, epithelial-derived mediators, such as interleukin (IL)-25, IL-33, thymic stromal lymphopoietin (TSLP) and ezrin, may play a role as alarmins in IL-4/IL-13 signaling in allergic asthma (AA).
The impact of the recombinantly produced IL-4 and IL-13 antagonist IL-4 mutein (IL-4M) on allergic sensitization and AIT outcome in experimental allergic asthma were analyzed in a murine model.
Further investigation showed that IL4 (interleukin 4), a key effector Th2 cytokine in allergic asthma, was critical for autophagy induction in B cells both in vivo and in vitro, which further sustained B cell survival and enhanced antigen presentation by B cells.
Increased IL-4- and IL-17-producing CD8<sup>+</sup> cells are related to decreased CD39<sup>+</sup>CD4<sup>+</sup>Foxp3<sup>+</sup> cells in allergic asthma.
This finding suggests that clinical events concerning neonatal IL-4 over-exposure, including neonatal hepatitis B vaccination and allergic asthma in human infants, may have adverse implications for brain development and cognition.
The SIT group, compared with the AA group, exhibited decreased sensitivity to the Der p allergen, concurrent with IL-4 down-modulation due to increased promoter DNA methylation, as estimated in PBMCs.
Results showed that compared with healthy children, levels of IL-9, IL-4 and PU.1 were elevated and levels of IFN-γ were lower in children with allergic asthma.
IL-4 signaling through the IL-4 receptor α (IL-4Rα) chain on CD4(+) T cells leads to TH2 cell differentiation in vitro, implying that IL-4Rα-responsive CD4(+) T cells are critical for the induction of allergic asthma.
Moreover, maternal stress can alter fetal cytokine balance, favoring TH2 (allergic) immune responses characteristic of atopic asthma: interleukin 6 (IL-6), which has been associated with premature labor, can promote TH2 responses by stimulating production of IL-4 and IL-13.
These results demonstrate an anti-lymphangiogenic function of TH2 cells and their cytokines, suggesting a potential usefulness of IL-4 and/or IL-13 antagonist as therapeutic agents for allergic asthma through expanding LV mediated-enhanced antigen clearance from the inflammatory sites.
The frequency of IL-4+IFN-gamma-IL-10-CD4+ cells (Th2) was significantly higher in the group with mild atopic asthma than in that with mild non-atopic asthma.
Association between the polymorphisms of IL-4 gene promoter (-590C>T), IL-13 coding region (R130Q) and IL-16 gene promoter (-295T>C) and allergic asthma.
Haplotype analysis showed a strong association between the IL4-34T/-589T haplotype and asthma per se (P=0.041), and a strong association between the IL4RA I50/Q576 haplotype and atopic asthma (P=0.006).