Mechanistically, naïve CD4+ T cells from obese mice showed increased LPC uptake, potentially explaining both the reduced circulating LPC 18:2 levels and its amplified pro-inflammatory effects in obese asthma.<h4>Conclusions</h4>Our findings highlight LPC 18:2 as a potential metabolic regulator that may link obesity-associated lipid disturbances to pathological Th17-skewed immune responses. The gene discussed is CD4; the disease is Obesity.