In male Th17 cells, androgen receptor (AR) signaling suppresses glutamine metabolism, resulting in mild allergic inflammation and reduced IL-17 production. The presence of androgens activates AR, which translocates to the nucleus and potentially regulates genes involved in glutamine metabolism, though the exact mechanism of AR-mediated suppression of glutamine metabolism remains to be fully elucidated. In contrast, female Th17 cells exhibit enhanced glutamine metabolism and severe allergic inflammation. The absence of AR signaling allows for increased glutamine (GLN) uptake through plasma membrane transporters and elevated glutaminase (GLS) activity. This leads to higher glutamate (Glu) production, which feeds into the TCA cycle and contributes to glutathione (GSH) synthesis. The enhanced glutamine metabolism in female Th17 cells correlates with increased IL-17 production and secretion, exacerbating allergic inflammation. Further research is needed to elucidate the precise molecular mechanisms linking enhanced glutamine metabolism to increased IL-17 production and Th17 cell pathogenicity in females, as the exact pathway has yet to be fully characterized.