With the evolution of novel biological therapies, patients, who do not-respond to conventional asthma therapy require novel biologic medications, such as anti-IgE, anti-IL-5 and anti-IL4/IL13 to control asthma symptoms.
The results indicated that IL-5 may involve in the pathologic process of asthma-like IL-4, and an inflammatory reaction may still exist in the airway during the remission stage of asthma.
The interaction of IL-5 with its receptor on eosinophils increases the activation and maintenance of eosinophils; blocking this interaction reduces asthma symptoms in patients with the eosinophilic phenotype.
An mAb directed against IgE (omalizumab) has become an established add-on therapy for patients with uncontrolled allergic asthma and mAbs specific for IL-5 (reslizumab, mepolizumab), IL-5R (benralizumab), and IL-4R (dupilumab) have been approved as add-on treatments for uncontrolled eosinophilic (type 2) asthma.
Th2 asthma is mediated by allergen-specific Th2 cells, and eosinophils activated by Th2 cells via the secretion of interleukin (IL)-4, IL-5, and IL-13.
IL-38 administration suppressed airway hyperreactivity and asthma-related IL-4 and IL-5 expression in humanized mice, together with significantly decreased CCR3<sup>+</sup> eosinophil numbers in the BALF and lungs, and a reduced percentage of human CD4<sup>+</sup>CRTH2<sup>+</sup> Th2 cells in the lungs and mediastinal lymph nodes.
Benralizumab, a humanized, anti-interleukin-5 (anti-IL-5) receptor α monoclonal antibody that directly and rapidly depletes eosinophils, has shown significant efficacy in reducing asthma exacerbations and improving lung function in moderate to severe eosinophilic asthma patients.
<b>Introduction</b>: The precision medicine approach that is now mandatory for severe asthma management includes the use of novel biologic agents blocking specific immunological mechanisms that are responsible for disease phenotypes and endotypes: monoclonal antibodies blocking IgE, IL-5 and IL-4/IL-13 immunological pathways are so far available.
All these IL-5 target drugs have been shown to reduce the number of exacerbation in patients with severe asthma selected on the basis of peripheral blood eosinophil count.
Stratification of patients with severe asthma by blood eosinophil counts predicts responders to anti-interleukin (IL)-5 (mepolizumab and reslizumab) and anti-IL-5 receptor α (benralizumab) therapies.
The current developments of the new biological drugs targeting interleukin 5 (IL-5) and IL-5 receptor allowed to expand the treatment options for severe hypereosinophilic asthma.
Group 2 innate lymphoid cells (ILC2s) and type 2 helper T (Th2) cells produce Th2 cytokines including IL-5 and play important roles in asthma pathogenesis.
We sought to target simultaneously the IL-4, IL-13, and IL-5 signaling pathways with a novel IL-4Rα/IL-5-bispecific antibody in a murine house dust mite (HDM) model of asthma.
Targeting eosinophils with anti-IL-5 therapy appears to be an exciting pathway in the properly selected patient with asthma and recent data also supports its use in COPD.
Recent clinical trials have demonstrated that targeting inflammatory pathways orchestrated through IL-4, IL-5, IL-13, and the prostaglandin receptor CRTH2 is potentially highly effective in adult asthma.
Its relative efficacy <i>versus</i> other IL-5-targeted treatments for patients with severe, uncontrolled asthma is not yet fully characterised.We performed a matching-adjusted indirect comparison (MAIC) of benralizumab <i>versus</i> mepolizumab and reslizumab.
Stimulation with IL-33 alone induced a significantly greater quantity of IL-13 by Lineage-cells from mugwort-allergic asthmatic compared with that from HDM-allergic asthmatics, whereas IL-25 induced a significantly greater amount of IL-5 by the Lineage-cells from mugwort-allergic asthmatic compared with that from HDM-allergic asthmatics.