Riprogrammazione metabolica e plasticità delle cellule ILC2 nella forma di asma correlata all'obesità.

Obesity-related asthma is a major clinical challenge defined by its unique pathology and resistance to corticosteroids. Here, we reframe this disease through the lens of tissue-specific "maladaptive plasticity" of group 2 innate lymphoid cells (ILC2s). We propose a central dichotomy: in the obese lung, mechanical transduction synergizes with metabolic inflammation to induce a HIF-1α-mediated glycolytic shift in ILC2s. Conversely, in visceral adipose tissue (VAT), chronic metabolic stress drives ILC2 functional exhaustion, suppressing cytokine secretion. This pulmonary glycolytic shift fuels acetyl-CoA accumulation and subsequent epigenetic remodeling, which locks ILC2s into a pathogenic ILC1