Biologic Therapies for Severe Eosinophilic Asthma

Summary

Severe eosinophilic asthma represents a distinct phenotype of asthma characterised by persistent symptoms, frequent exacerbations and elevated eosinophil counts despite high‐dose inhaled corticosteroids and other controller medications. Biologic therapies have transformed management by targeting key mediators of type 2 inflammation. Monoclonal antibodies directed against interleukin-5 (IL-5) or its receptor (IL-5Rα) can reduce eosinophil survival and activation, thereby lowering exacerbation frequency and improving lung function. Alternative approaches include antagonists of upstream alarmins such as thymic stromal lymphopoietin (TSLP) and inhibitors of interleukin-4/13 signalling, broadening treatment across phenotypic subgroups. Choice of agent is guided by biomarkers such as blood eosinophil count, fraction of exhaled nitric oxide and specific comorbidities. Head-to-head comparisons remain scarce, and real-world evidence highlights variability in individual responses, driving interest in precision medicine. The global impact of these therapies extends beyond clinical endpoints to reduced oral corticosteroid dependence and healthcare utilisation. Ongoing work seeks novel biomarkers to refine patient selection and to explore combination or sequential use of biologics in refractory cases.

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Biologic Therapies for Severe Eosinophilic Asthma publication trend

The graph below shows the total number of articles in biologic therapies for severe eosinophilic asthma across all publications each year (not limited to Nature Index journals).

Technical terms

Eosinophil: A type of white blood cell involved in allergic inflammation and asthma exacerbations.

Interleukin-5 (IL-5): A cytokine essential for eosinophil differentiation, activation and survival.

IL-5 receptor (IL-5Rα): Cell‐surface receptor binding IL-5, targeted by receptor-directed antibodies.

Monoclonal antibody: A laboratory-engineered protein designed to bind specifically to a molecular target.

Type 2 inflammation: Immune response characterised by cytokines IL-4, IL-5 and IL-13, associated with allergic asthma.

Alarmin: An epithelial‐derived cytokine released in response to environmental insults, initiating type 2 immune cascades (e.g., TSLP).

References

  1. Targeting the IL‐5 pathway in eosinophilic asthma: A comparison of anti‐IL‐5 versus anti‐IL‐5 receptor agents. Allergy (2024).
  2. Long-Term Therapy Response to Anti–IL-5 Biologics in Severe Asthma—A Real-Life Evaluation. The Journal of Allergy and Clinical Immunology In Practice (2020).
  3. Real‐world efficacy of treatment with benralizumab, dupilumab, mepolizumab and reslizumab for severe asthma: A systematic review and meta‐analysis. Clinical & Experimental Allergy (2022).
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