Interleukin-5 Targeting in Eosinophilic Asthma
Summary
Eosinophilic asthma is characterised by excessive airway inflammation driven by the cytokine interleukin-5 (IL-5), which governs the growth, survival and activation of eosinophils. In susceptible individuals, elevated IL-5 levels promote eosinophil recruitment to the bronchial mucosa, leading to airway hyper-responsiveness, mucus overproduction and tissue remodelling. Conventional therapies such as inhaled corticosteroids may inadequately control severe eosinophilic asthma, leaving patients at risk of frequent exacerbations and systemic corticosteroid dependence. Targeted interventions have therefore been developed to neutralise IL-5 or block its receptor. Monoclonal antibodies directed against IL-5 (for example mepolizumab and reslizumab) reduce circulating and tissue eosinophil counts, whereas agents targeting the IL-5 receptor α-chain (for example benralizumab) induce antibody-dependent cell cytotoxicity to deplete eosinophils more rapidly. Clinical outcomes of these biologics include marked reductions in exacerbation rates, improved lung function and the possibility of tapering oral corticosteroids. Ongoing research seeks to refine patient selection, identify biomarkers of response and understand the long-term impact on airway remodelling and comorbid conditions such as nasal polyposis.
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Interleukin-5 Targeting in Eosinophilic Asthma publication trend
The graph below shows the total number of articles in interleukin-5 targeting in eosinophilic asthma across all publications each year (not limited to Nature Index journals).
Technical terms
Interleukin-5 (IL-5): A cytokine that specifically promotes eosinophil differentiation, activation and survival.
Eosinophils: A subset of white blood cells involved in type 2 inflammation and allergic responses, central to asthma pathogenesis.
Monoclonal antibody: A laboratory-engineered protein that recognises a single antigenic target, used here to neutralise IL-5 or its receptor.
Benralizumab: A monoclonal antibody against the IL-5 receptor α-chain, inducing eosinophil apoptosis via antibody-dependent cell cytotoxicity.
Mepolizumab/Reslizumab: Monoclonal antibodies that bind IL-5, preventing its interaction with the eosinophil receptor.
Exacerbation: An acute worsening of asthma symptoms typically requiring systemic corticosteroids or hospitalisation.
Type 2 (T2) inflammation: An immune-response pattern driven by Th2 cells and associated cytokines (IL-4, IL-5, IL-13) characteristic of eosinophilic asthma.
References
- IL-5 antagonism reverses priming and activation of eosinophils in severe eosinophilic asthma. Mucosal Immunology (2024).
- Sustained remission induced by 2 years of treatment with benralizumab in patients with severe eosinophilic asthma and nasal polyposis. Respirology (2024).
- Achieving clinical outcomes with benralizumab in severe eosinophilic asthma patients in a real-world setting: ORBE II study. Respiratory Research (2023).
- Interleukin-5 in the Pathophysiology of Severe Asthma. Frontiers in Physiology (2019).
- Benralizumab: From the Basic Mechanism of Action to the Potential Use in the Biological Therapy of Severe Eosinophilic Asthma. BioMed Research International (2018).
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