In the current report, we examine whether combined blockade of IL-13 and IL-17A, at individually sub-therapeutic levels, can limit the development of allergic asthma while sparing expression of IL-17A-associated anti-microbial effectors.
Interestingly, the occurrence of AA elevates the plasma levels of leptin, and this adipokine was positively correlated with the release of IL-5, IL-6 and IL-17, but inversely correlated with IL-10 production, by CD4<sup>+</sup> T-cells from patients.
IL-4 and IL-13 levels were significantly higher at baseline in the AA group compared with HS and, after allergen exposure, were significantly increased in the AA group, with no effect on HS.
In this review, we focus on the recent advances of the underlying intercellular and intracellular mechanisms by which IL-33 can regulate the allergic inflammation in various allergic diseases including allergic asthma and atopic dermatitis.
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.
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.
The serum level of IL-33 at baseline was significantly higher in the AA group compared with HS, but the allergen challenge did not provoke an increase of this cytokine in any group.
In the current report, we examine whether combined blockade of IL-13 and IL-17A, at individually sub-therapeutic levels, can limit the development of allergic asthma while sparing expression of IL-17A-associated anti-microbial effectors.
In those patients, higher levels of IL-5, IL-6 and IL-17 were quantified in CD4<sup>+</sup> T-cell cultures as compared with patients with mild and moderate AA.
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.
Recently, IL-33 has been implicated in shaping the immune system of the lungs early in life, at a time which is crucial in the subsequent development of allergic asthma.
Inhaled CDP7766 potently inhibited the function of IL-13 generated during the airway response to inhaled allergen in cynomolgus macaques, demonstrating the potential of inhaled anti-IL-13 therapeutics for the treatment of allergic asthma.
Our findings unveil the "protease-FCP-TLR4-mast cell-IL-13" axis as a molecular mechanism for generation of T<sub>H</sub>2-favorable PD-L2<sup>+</sup> DCs in allergic asthma and suggest that targeting the PD-L2<sup>+</sup> DC pathway might be effective in suppressing allergic T-cell responses in the airway.