LTC₄/CysLT₂

LTC₄/CysLT₂ (CYSLTR2) is a cysteinyl leukotriene signaling axis that regulates inflammatory and vascular responses through a G protein-coupled receptor predominantly coupled to Gq/11-dependent signaling pathways^[3][4]. CysLT₂ functions as a receptor for cysteinyl leukotrienes and contributes to leukotriene-induced modulation of smooth muscle contraction, vascular permeability, and leukocyte activation, placing this pathway at the center of allergic and inflammatory biology^[3]. Mechanistically, LTC₄ activates CysLT₂-dependent cellular responses, including calcium signaling in endothelial cells and cytokine-associated inflammatory programs in immune cells and platelets^[5][6][1]. In disease settings, CysLT₂ signaling has been linked to eosinophilic type 2 immunopathology, aspirin-exacerbated respiratory disease-like inflammation, dermatitis-associated itch responses, and allergic airway disorders^[1][2][7]. Compared with the closely related CysLT₁ receptor, CysLT₂ displays distinct pharmacological and biological properties; CysLT₂ can negatively regulate CysLT₁-dependent pulmonary Th2 inflammation, and several classical CysLT₁ antagonists, including montelukast, show little or no activity at CysLT₂^[3][6]. This functional divergence is important for experimental design because receptor-selective signaling may influence inflammatory outcomes independently of CysLT₁ pathways^[6]. For research applications, selective CysLT₂ antagonists have been reported to block vascular permeability and myocardial ischemia/reperfusion injury in experimental models, providing useful tools for mechanistic studies of leukotriene biology and inflammatory disease processes^[3].