What is it about?

This study investigates the genetic factors that make asthma more severe in some patients than in others. The researchers analyzed the DNA of 169 Japanese adults with asthma to identify specific genetic variations (polymorphisms) in immune system genes. Key Findings: A Specific Risk Factor: The study identified that a specific variation in the IL1RL1 gene (called the rs11685480 “A” allele) is a significant risk factor for severe asthma. The Mechanism: This genetic variation changes how the immune system behaves in two ways: 1. It increases the number of receptors (IL1RL1 mRNA) on T cells that receive signals for inflammation. 2. It decreases the levels of a protective “decoy” protein (soluble ST2) in the blood that usually blocks those inflammation signals. The Result: This combination leads to stronger inflammation (Type 2 inflammation), characterized by higher levels of nitric oxide in the breath and more eosinophils (a type of white blood cell) in the blood.

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Why is it important?

Severe asthma is a difficult condition that causes frequent attacks and significantly lowers a patient’s quality of life. Understanding the “why” behind disease severity is crucial for improving patient care. Better Understanding: This research clarifies the biological mechanism—specifically the IL-33/IL1RL1 signaling pathway—that drives severe inflammation in asthma patients. New Treatments: By confirming that this pathway drives severity, the study suggests that medical treatments targeting IL-33 and its receptors could be very effective for patients with severe asthma. Personalized Medicine: It helps move medicine toward “stratification,” where doctors can predict who might get severe asthma based on their genes and treat them accordingly.

Perspectives

Genetic Influence: This study reinforces the idea that a person’s genetics play a major role in how their immune system responds and how severe their asthma becomes. Therapeutic Potential: The findings support the development of drugs that can block the IL-33 signal or mimic the “decoy” receptor to reduce inflammation. Future Research: Because this study was conducted specifically among Japanese patients, further research is needed to determine whether these genetic links exist in other populations worldwide. Additionally, more work is needed to understand exactly how this genetic change functions at a cellular level.

Keita Hirai
Shinshu Daigaku

Read the Original

This page is a summary of: IL1RL1 rs11685480 polymorphism is associated with IL-33/IL1RL1 pathway activity and asthma severity in a Japanese population, Respiratory Investigation, January 2026, Elsevier,
DOI: 10.1016/j.resinv.2025.101362.
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