Herpesvirus entry mediator (HVEM) and Lymphotoxin beta receptor (LTβR) (HVEM (for Herpesvirus entry mediator), LTβR (for Lymphotoxin beta receptor))

Herpesvirus entry mediator (HVEM) and Lymphotoxin beta receptor (LTβR) are both members of the tumor necrosis factor receptor superfamily. HVEM (TNFRSF14) functions as a hub integrating signals from multiple ligands, including LIGHT (TNFSF14), BTLA, and CD160, controlling both costimulatory and inhibitory signaling cascades vital to T and B cell activation, survival, and immune homeostasis[1][3]. It is also involved in viral pathology, serving as an entry receptor for herpes simplex virus. LTβR (TNFRSF3) primarily binds lymphotoxin-α1β2 and LIGHT, orchestrating the development and maintenance of lymphoid organs, regulation of immune responses, inflammatory signaling, and apoptotic pathways[4][5]. Both receptors play significant roles in immune signaling networks, are being explored as therapeutic targets in cancer, autoimmune and inflammatory diseases, and are integral to maintaining proper lymphoid tissue architecture and immune cell function[1][2][4][5].

Other names

HVEM: Tumor necrosis factor receptor superfamily member 14 (TNFRSF14), HveALTβR: Lymphotoxin-beta receptor, Tumor necrosis factor receptor superfamily member 3 (TNFRSF3), LTBR

Blockade or activation of ligand–receptor interactions (e.g., inhibition of LIGHT binding to HVEM/LTβR) Modulation of downstream NF-κB signaling pathways Regulation of immune cell activation or suppression (costimulation or coinhibition) Induction of apoptosis or enhancement of cell survival, depending on cellular context