In a significant step forward in asthma research, Canadian scientists from McMaster University in Ontario have identified a new population of immune cells in the airways of individuals with severe asthma that can worsen the condition.
Their study, “A Population of c-kit+ IL-17A+ ILC2s in Sputum From Individuals With Severe Asthma Supports ILC2 to ILC3 Trans-Differentiation,” was recently published in Science Translational Medicine. Researchers have called the immune cells chameleon-like, as they exhibit traits and change characteristics between both group 2 innate lymphoid cells (ILC2s) and group 3 innate lymphoid cells (ILC3s).
Detecting the cells in the sputum of individuals with severe asthma, researchers revealed the cells’ strong correlation with airway neutrophilia, one of four phenotypes of severe asthma, and elevated levels of inflammatory cytokines IL-1β and IL-18. In vitro experiments demonstrated that canonical ILC2s could up-regulate c-kit and IL-17A when cultured with IL-1β and IL-18, suggesting a potential for these cells to trans-differentiate in response to specific inflammatory signals.
Implications from the study suggest the intermediate ILC2 population represents a potential therapeutic target for controlling neutrophilic airway inflammation in severe asthma. Additionally, understanding the immunological basis of different asthma phenotypes can help develop personalized treatment strategies to improve symptom control and reduce exacerbations.
According to researchers, although most cases of asthma are well-managed with standard treatments, a significant subset of patients with severe asthma continues to experience uncontrolled symptoms despite high-dose corticosteroid therapy. The study indicated future research will focus on further characterizing these cells and exploring targeted therapies to improve outcomes for patients with severe asthma.
