The article focuses on the metabolic vulnerabilities of immune cells involved in allergic airway diseases like asthma. The study investigates how allergen-induced Innate Lymphoid Cells (ILC2s) and T helper type 2 (Th2) cells adapt their metabolism to survive in inflammatory environments. A central finding is that these pathogenic cells rely on cystine-driven glutathione (GSH) synthesis to activate antioxidant systems, specifically GPX4 and TXNRD1, which confer resistance to a type of cell death called ferroptosis by counteracting toxic lipid peroxidation. This redox balance is essential for the cells to acquire and utilize lipids for expansion and function. Ultimately, the research proposes that targeting this metabolic vulnerability, particularly the TXNRD1 system, may be an effective therapeutic strategy to restrain chronic airway inflammation.
References:
- Wientjens C, Doverman M, Zurkovic J, et al. Tolerance to ferroptosis facilitates lipid metabolism and pathogenic type 2 immunity in allergic airway inflammation[J]. Immunity, 2025.
