Therapeutic Strategies in Allergic Airway Inflammation

Allergic airway inflammation underpins conditions such as asthma and allergic rhinitis, in which inhaled allergens trigger a type 2 immune cascade leading to bronchoconstriction, mucus hypersecretion and airway remodelling. Traditional management relies on inhaled corticosteroids and bronchodilators to suppress inflammation and relieve symptoms, but a substantial proportion of patients remain poorly controlled or experience steroid-related adverse effects. Over the past decade, a precision-medicine approach has emerged, targeting specific mediators of the type 2 pathway, including interleukin-4, interleukin-5 and immunoglobulin E. Monoclonal antibodies directed against these cytokines or their receptors have demonstrated significant reductions in exacerbation rates and oral steroid use in selected phenotypes. Parallel efforts have explored small-molecule inhibitors of intracellular kinases such as Janus kinases (JAKs) and phosphoinositide 3-kinase delta (PI3Kδ), which modulate T-cell activation and cytokine signalling. Preclinical and early-phase clinical studies have also evaluated oligonucleotide therapeutics to silence pro-inflammatory genes, and novel biologics targeting epithelial alarmins such as thymic stromal lymphopoietin. Future strategies integrate biomarker-driven patient stratification with combination regimens of biologics and small molecules, aiming to address steroid-resistant and non-type-2 endotypes and to achieve sustained disease modification.

Research from Nature Portfolio

No recent Nature Portfolio content available.

Therapeutic Strategies in Allergic Airway Inflammation publication trend

The graph below shows the total number of articles in therapeutic strategies in allergic airway inflammation across all publications each year (not limited to Nature Index journals).

Technical terms

Type 2 inflammation: An immune response driven by Th2 cells and type 2 innate lymphoid cells, characterised by interleukins 4, 5 and 13 and eosinophil recruitment.

Monoclonal antibody: A laboratory-produced protein engineered to bind a specific cytokine or receptor, thereby neutralising its activity.

JAK inhibitor: A small molecule that blocks Janus kinase enzymes, interrupting cytokine receptor signalling cascades within immune cells.

Airway hyperresponsiveness: An exaggerated bronchoconstrictive response to stimuli, leading to airflow limitation.

Eosinophilia: An elevated concentration of eosinophils in blood or airway tissues, often reflective of type 2-mediated inflammation.

References

1. Type 2 inflammation and biological therapies in asthma: Targeted medicine taking flight. Journal of Experimental Medicine (2023).
2. Anti-inflammatory potential of PI3Kδ and JAK inhibitors in asthma patients. Respiratory Research (2016).
3. Biological therapy for severe asthma. Asthma Research and Practice (2021).
4. Oligonucleotide Therapy for Obstructive and Restrictive Respiratory Diseases. Molecules (2017).
5. Strategies Targeting Type 2 Inflammation: From Monoclonal Antibodies to JAK-Inhibitors. Biomedicines (2021).
6. Ruxolitinib Ameliorates Airway Hyperresponsiveness and Lung Inflammation in a Corticosteroid-Resistant Murine Model of Severe Asthma. Frontiers in Immunology (2021).
7. Which Therapy for Non-Type(T)2/T2-Low Asthma. Journal of Personalized Medicine (2021).