TNFRSF3/CD18

TNFRSF3/CD18, also known as LTβR, is a lymphotoxin-β-specific TNF receptor that supports cell-surface lymphotoxin biology distinct from secreted LTα^[1]. Mechanistically, LTβR activates classical and alternative NF-κB signaling, including NF-κB2/p100 processing to p52 through NIK and IKKα^[2]. In immune tissue models, LTβR deficiency disrupts Peyer’s patches, lymph nodes, follicular dendritic cell networks, and affinity maturation in peripheral lymphoid tissues^[3][4]. Compared with soluble LTα signaling, LTβR primarily interprets membrane LTα1β2 and LIGHT/TNFSF14 inputs, linking stromal-cell signaling to lymphoid organogenesis and inflammatory microarchitecture^[1][3][4]. For experimental applications, soluble LTβR-Ig suppresses LTβR-dependent follicular dendritic cell markers and germinal-center activity, while LIGHT-driven LTβR activation can mediate tumor-cell apoptosis in defined models^[5][6].