LILRB

Leukocyte immunoglobulin-like receptor B (LILRB) family members act as inhibitory immune receptors that regulate cellular activation through immunoreceptor tyrosine-based inhibitory motifs (ITIMs)^[1][2][3]. LILRB4 specifically suppresses monocyte and dendritic cell activation by recruiting phosphatases such as SHP1 and modulating NF-κB and MAPK signaling pathways^[1][4][5]. Mechanistically, LILRB4 restrains antigen-bearing dendritic cell migration and reduces Th2-mediated pulmonary inflammation in experimental models^[6][7]. In cardiovascular and hepatic disease models, LILRB4 overexpression mitigates cardiac hypertrophy, fibrosis, and inflammation, and attenuates nonalcoholic fatty liver disease by inhibiting NF-κB and TRAF6-dependent signaling^[8][9][4]. Compared with LILRB1 and LILRB2, LILRB4 displays distinct tissue-specific expression, with predominant activity in monocytes, dendritic cells, and hepatocytes, allowing selective modulation of inflammatory and metabolic responses^[1][4][10]. Agonistic or overexpression strategies of LILRB4 confer protective effects in models of cardiac, hepatic, and intestinal injury, whereas LILRB4 deficiency exacerbates pathological remodeling and inflammatory responses^[8][9][5]. These functional distinctions underscore the receptor’s potential as a therapeutic target in inflammatory, metabolic, and immunopathological conditions, with applications in both experimental mechanistic studies and preclinical intervention designs^[8][4][5].

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