LILRB1

Leukocyte immunoglobulin-like receptor B1 (LILRB1) functions as an inhibitory immune checkpoint that modulates neutrophil activation and migration^[1]. Mechanistically, LILRB1 attenuates neutrophil extracellular trap (NET) formation by suppressing pro-inflammatory cytokine release, including IL-1β, IL-6, and IL-8, in drug-resistant Pseudomonas aeruginosa-associated bronchiectasis^[1]. This receptor operates through interactions with soluble HLA-G, with inverse correlations observed between LILRB1 expression and disease severity indices or peripheral neutrophil counts^[1]. Compared with related inhibitory receptors, LILRB1 uniquely regulates neutrophil migration in co-culture models, reducing chemotactic responses toward infected bronchial epithelial cells^[1]. Experimental applications of recombinant LILRB1 protein demonstrate suppression of NETosis and inflammatory cytokine production, highlighting its potential as a modulatory agent in neutrophil-driven airway inflammation^[1]. In addition, LILRB1 signaling may converge with PI3K/Akt/mTOR pathways, consistent with inhibitory roles observed in axonal outgrowth and immune cell regulation, although direct mechanistic links remain under investigation^[2]. Collectively, LILRB1 serves as a critical checkpoint in neutrophil-mediated inflammation, providing a framework for studying immunomodulatory interventions and selective agonist or inhibitory strategies in respiratory disease models^[1][2].