The lymphotoxin-beta receptor (LTβR), a member of the tumor necrosis factor (TNF) receptor superfamily, is broadly expressed on stromal, endothelial, and myeloid cells within the TME and signals through both canonical and non-canonical NF-κB pathways.
First-pass extracted concept
lymphotoxin-beta receptor
Aliases
LTβR
Evidence Snippets
Supporting Sources
Linked Claims
Selective LTβR modulation may synergize with immune checkpoint blockade and CAR T cell therapies to overcome immunotherapy resistance in refractory solid tumors.
Persistent LTβR signaling supports immunosuppressive macrophage phenotypes and promotes tumor growth in hepatocellular carcinoma.
Depending on context and activation mode, LTβR can drive either tumor progression or anti-tumor immunity.
LTβR signals through both canonical and non-canonical NF-κB pathways.
In preclinical colorectal and cervical cancer models, LTβR activation induces tertiary lymphoid structures, high endothelial venules, and immune infiltration, improving responsiveness to immune checkpoint blockade.