iNKT Cell Activation by Fungal Glycosphingolipid Asperamide B and Its Role in Asthma ID: 2013-055

This study unveils a novel mechanism by which the fungal glycosphingolipid asperamide B from *Aspergillus fumigatus* activates iNKT cells, leading to airway hyperreactivity, a key feature of asthma.

Technology Overview

The research conducted by Brigham Young University details how asperamide B, a compound derived from *Aspergillus fumigatus*, can induce airway hyperreactivity by directly activating invariant natural killer T (iNKT) cells. This process occurs through a CD1d-restricted, MyD88-independent mechanism, specifically engaging an IL-33-ST2-dependent pathway. This groundbreaking discovery is the first to identify a fungal glycolipid capable of directly activating iNKT cells, offering new insights into the pathogenesis of asthma and potential therapeutic targets.

Key Advantages

• First identification of a fungal glycolipid directly activating i
• NKT cells
• Elucidation of a novel IL-33-ST2-dependent pathway for airway hyperreactivity induction
• Provides a potential explanation for high rates of *A
• fumigatus* sensitization in severe asthma patients
• Expands understanding of i
• NKT cell activation beyond bacteria and viruses to include fungi

Problems Addressed

• Uncovers a previously unknown mechanism of asthma pathogenesis
• Addresses the gap in understanding the role of i
• NKT cells in allergic diseases and asthma
• Offers new avenues for research into therapeutic interventions targeting i
• NKT cell activation

Market Applications

• Development of novel therapeutic agents targeting the IL-33-ST2 pathway
• Creation of diagnostic tools for identifying susceptibility to asthma based on i
• NKT cell activity
• Pharmaceutical interventions aimed at inhibiting asperamide B and similar fungal glycolipids

Additional Information

Technology ID: 2013-055
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Date Published: 13 May, 2025