Affinage

LTBR

Tumor necrosis factor receptor superfamily member 3 · UniProt P36941

Round 2 corrected
Length
435 aa
Mass
46.7 kDa
Annotated
2026-04-28
40 papers in source corpus 20 papers cited in narrative 21 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

LTBR (lymphotoxin-beta receptor / TNFRSF3) is a TNF receptor superfamily member that transduces signals from the LTα1β2 heterotrimer and LIGHT (TNFSF14) to orchestrate lymphoid tissue organization, inflammatory gene expression, and cell death (PMID:8171323, PMID:9462508). Upon ligand engagement, LTBR recruits TRAF3 to propagate apoptotic signaling and TRAF2/TRAF5 to activate two distinct NF-κB arms: a canonical IKKβ/NEMO-dependent pathway driving proinflammatory genes and a non-canonical NIK/IKKα-dependent pathway that processes p100 to p52/RelB and induces lymphoid organogenesis chemokines, with NIK/IKKα also phosphorylating p65 at Ser536 to enhance transcriptional activation (PMID:9122217, PMID:8663299, PMID:12387745, PMID:12419817). In vivo, LTBR signaling is required for tertiary lymphoid structure formation and maintenance, drives hepatitis-associated hepatocellular carcinoma through hepatocyte IKKβ, sustains immunosuppressive M2 macrophage polarization via non-canonical NF-κB and Wnt/β-catenin, and—when activated by tumor-targeted LIGHT or FAP-directed agonists—remodels the tumor microenvironment to promote T cell infiltration and enhance immunotherapy efficacy (PMID:16934497, PMID:19800575, PMID:39429877, PMID:26977880, PMID:42012453). Therapeutic blockade of LTBR in lung tissue disrupts inducible bronchus-associated lymphoid tissue and activates WNT/β-catenin-driven alveolar regeneration, reversing airway fibrosis in COPD models (PMID:33149305).

Mechanistic history

Synthesis pass · year-by-year structured walk · 9 steps
  1. 1994 High

    Identifying the receptor for surface lymphotoxin established that LTα/LTβ heteromeric complexes signal through a dedicated receptor (LTBR) distinct from the TNF receptors that bind soluble LTα homotrimers, defining a new branch of TNF superfamily signaling.

    Evidence Receptor binding assays with purified LTα/LTβ heteromers

    PMID:8171323

    Open questions at the time
    • Stoichiometry of the LTα/LTβ:LTBR complex not determined
    • Intracellular signaling mechanism unknown at this point
  2. 1997 High

    Mapping the adaptor recruitment profile of LTBR revealed that TRAF3 mediates LTBR-induced cell death while TRAF2 and TRAF5 contribute to NF-κB activation, establishing that LTBR bifurcates into independent death and transcriptional signaling arms through distinct TRAF proteins.

    Evidence Co-immunoprecipitation, dominant-negative TRAF3/TRAF5 mutants, NF-κB reporters, and cell death assays in multiple cell types

    PMID:7859281 PMID:8663299 PMID:9122217

    Open questions at the time
    • Precise TRAF binding motifs on the LTBR cytoplasmic tail not resolved
    • Whether other adaptors participate in either arm remained open
  3. 1998 High

    Discovery that LIGHT (TNFSF14) is a second ligand for LTBR, independent of LTα/LTβ, expanded the receptor's functional repertoire and revealed regulation by decoy receptor DcR3, providing a framework for how LTBR signaling is tuned by ligand competition.

    Evidence Receptor-ligand binding assays, functional blocking, cytotoxicity assays with recombinant LIGHT and DcR3

    PMID:10318773 PMID:10799510 PMID:9462508

    Open questions at the time
    • Relative physiological contribution of LIGHT versus LTα1β2 in different tissues unclear
    • Structural basis of ligand selectivity not determined
  4. 2002 High

    Demonstrating that LTBR activates two mechanistically distinct NF-κB pathways—canonical IKKβ/NEMO-dependent (proinflammatory genes) and non-canonical NIK/IKKα-dependent (p100→p52 processing, lymphoid chemokines)—with an additional NIK/IKKα-mediated p65-Ser536 phosphorylation step, resolved how a single receptor drives both acute inflammation and lymphoid organogenesis programs.

    Evidence Genetic epistasis in IKK-deficient MEFs, dominant-negative kinases, site-directed mutagenesis of p65-Ser536, chemokine expression profiling

    PMID:12387745 PMID:12419817

    Open questions at the time
    • Temporal kinetics of the two pathways in vivo not resolved
    • Contribution of p65-Ser536 phosphorylation versus p52/RelB to specific gene targets uncharacterized
  5. 2006 High

    Showing that LTBR signaling is necessary and sufficient for tertiary lymphoid organ (TLO) formation in vivo linked the non-canonical NF-κB chemokine program to organized ectopic lymphoid tissue development and autoimmune pathology.

    Evidence In vivo LIGHT blockade and islet-specific LIGHT transgenic mice in NOD diabetes model

    PMID:16934497

    Open questions at the time
    • Cell-type-specific contributions of stromal versus immune LTBR in TLO maintenance not dissected
    • Signals distinguishing protective versus pathogenic TLOs unknown
  6. 2009 High

    Establishing that chronic hepatic LTα/LTβ–LTBR signaling drives HCC through hepatocyte IKKβ, independent of TNFR1, identified LTBR as a direct oncogenic driver in inflammation-associated liver cancer.

    Evidence Liver-specific LTαβ transgenic mice, IKKβ and TNFR1 genetic knockouts, in vivo LTβR blockade

    PMID:19800575

    Open questions at the time
    • Downstream IKKβ target genes mediating hepatocyte transformation not fully catalogued
    • Whether LTBR blockade can reverse established HCC not tested
  7. 2016 High

    Tumor-targeted delivery of LIGHT demonstrated that activating LTBR signaling in the tumor stroma generates T cell-recruiting chemokines sufficient to overcome checkpoint blockade resistance, establishing LTBR agonism as a strategy for converting immune-cold tumors.

    Evidence Antibody-LIGHT fusion protein in syngeneic tumor models with combination anti-PD-L1 therapy

    PMID:26977880

    Open questions at the time
    • Relative contribution of LTBR versus HVEM to LIGHT-mediated immune remodeling in tumors not separated
    • Optimal LTBR engagement thresholds for efficacy versus toxicity unknown
  8. 2020 High

    Demonstrating that LTBR blockade disrupts pathogenic iBALT, suppresses non-canonical NF-κB/TGFβ, and activates WNT/β-catenin-driven lung regeneration revealed LTBR as a therapeutic target in COPD and established a previously unrecognized connection between lymphotoxin signaling and epithelial progenitor cell fate.

    Evidence In vivo LTβR blocking in aged and cigarette-smoke-exposed mice, WNT reporter assays, validation in human COPD tissue

    PMID:33149305

    Open questions at the time
    • Mechanism by which LTBR suppresses WNT signaling not molecularly defined
    • Long-term safety of LTBR blockade for regenerative therapy not assessed
  9. 2024 Medium

    Cell-type-specific studies revealed that LTBR maintains immunosuppressive M2 macrophage polarization via non-canonical NF-κB/Wnt/β-catenin and that FAP-targeted LTBR agonism selectively activates endothelial cells to form TLS-like aggregates, refining the understanding of how LTBR controls different immune–stromal compartments in the tumor microenvironment.

    Evidence Macrophage-specific conditional LTBR knockout, TAM-targeted siRNA delivery, FAP-LTBR bispecific agonist in 3D microfluidic models and murine tumors, spatial transcriptomics

    PMID:39164890 PMID:39429877 PMID:42012453

    Open questions at the time
    • How LTBR agonism and antagonism in different cell types can be simultaneously exploited therapeutically is unresolved
    • Whether macrophage LTBR signaling is relevant in non-tumor inflammatory settings not tested
    • Findings from single labs await independent replication

Open questions

Synthesis pass · forward-looking unresolved questions
  • Unresolved: the structural basis of LTBR signal complex assembly (TRAF stoichiometry, conformational activation), the precise molecular mechanism linking LTBR to WNT/β-catenin suppression, and the determinants separating protective (anti-tumor TLS) from pathogenic (autoimmune TLO, HCC-promoting) outcomes of LTBR signaling remain undefined.
  • No crystal or cryo-EM structure of LTBR signaling complex
  • Molecular intermediates between LTBR and WNT pathway not identified
  • Context-dependent rules governing beneficial versus harmful LTBR activation not established

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060089 molecular transducer activity 3 GO:0060090 molecular adaptor activity 3
Localization
GO:0005886 plasma membrane 4
Pathway
R-HSA-162582 Signal Transduction 7 R-HSA-168256 Immune System 4 R-HSA-5357801 Programmed Cell Death 4 R-HSA-1643685 Disease 2 GO:0005886 plasma membrane 1
Partners
LTALTBTNFRSF6BTNFSF14TRAF1TRAF2TRAF3TRAF5

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1994 Identification of LTBR (lymphotoxin-beta receptor) as a receptor specific for the LT-alpha/LT-beta heteromeric complex on the cell surface, distinct from the p60 and p80 TNF receptors that bind secreted LT-alpha homotrimers. Receptor binding assay / protein biochemistry Science High 8171323
1995 TRAF2 (LAP1) and TRAF1 (EBI6) associate with the cytoplasmic domain of LTBR; EBV LMP1 co-immunoprecipitates with these TRAF proteins and causes them to localize to LMP1 clusters in the plasma membrane, linking LMP1 transformation to TNFR-family signaling including LTBR. Co-immunoprecipitation, immunofluorescence localization Cell High 7859281
1996 TRAF5 binds specifically to the cytoplasmic region of LTBR (but not CD40, TNFR1, TNFR2, Fas, or NGFR) in vitro and co-immunoprecipitates with LTBR when overexpressed in COS7 cells; TRAF5 overexpression activates NF-κB and a dominant-negative truncated TRAF5 partially inhibits LTbetaR-induced NF-κB activation. In vitro translation binding assay, co-immunoprecipitation in COS7 cells, NF-κB reporter assay The Journal of biological chemistry High 8663299
1997 TRAF3 is rapidly recruited to the LTBR cytoplasmic domain upon LT-alpha1/beta2 or agonistic anti-LTBR antibody treatment; dominant-negative TRAF3 (lacking RING and zinc finger domains) specifically inhibits LTBR-mediated cell death but not NF-κB activation, establishing TRAF3 as a critical component of the LTBR death-signaling complex and demonstrating two independent signaling pathways downstream of LTBR. Co-immunoprecipitation, stable overexpression of dominant-negative mutant, cell death assay Proceedings of the National Academy of Sciences of the United States of America High 9122217
1997 HCV core protein directly binds the cytoplasmic tail of LTBR; the binding site on LTBR was mapped to a 58-amino-acid region of its cytoplasmic tail and the HCV core binding site was localized to residues 36–91 (hydrophilic region); association was confirmed in mammalian cells by co-immunoprecipitation. Yeast two-hybrid screen, GST pull-down assay, protein-protein blotting, mammalian co-immunoprecipitation Journal of virology High 8995654
1998 LIGHT (TNFSF14), a new TNF superfamily member produced by activated T cells, binds both HVEM and LTBR (the LT-alpha/beta heterotrimer receptor); LIGHT does not form complexes with LT-alpha or LT-beta and HSV gD inhibits HVEM-LIGHT interaction, establishing LIGHT as a dual-receptor ligand in the lymphotoxin system. Receptor-ligand binding assays, transfection, functional blocking studies Immunity High 9462508
1999 Decoy receptor 3 (TR6/DcR3) specifically binds LIGHT and FasL; TR6 inhibits LIGHT-induced cytotoxicity by blocking LIGHT interactions with both LTBR and HVEM, suppressing LIGHT-mediated apoptosis in HT29 cells that express both receptors. Immunoprecipitation of recombinant proteins, flow cytometry, cytotoxicity assay The Journal of biological chemistry High 10318773
2000 LTBR (not HVEM) is necessary and sufficient for LIGHT-mediated apoptosis and ICAM-1 induction; LIGHT mutants with selective HveA binding cannot trigger cell death; LTBR (not HveA) recruits TRAF3, and dominant-negative TRAF3 blocks LIGHT-induced death, establishing TRAF3 recruitment as the mechanism propagating LTBR death signals. Point mutagenesis of LIGHT, receptor-specific antibody blocking, dominant-negative TRAF3 overexpression, cell death assay The Journal of biological chemistry High 10799510
2002 LTBR ligation activates two distinct NF-κB pathways: (1) canonical IKKβ/NEMO-dependent NF-κB driving proinflammatory genes (VCAM-1, MIP-1β, MIP-2) and expression of p100; (2) non-canonical NIK/IKKα-dependent processing of NF-κB2/p100 to p52 (independent of NEMO/IKKγ), driving lymphoid organogenesis chemokines (SLC, BLC, ELC, SDF1, BAFF). Genetic epistasis using IKK-deficient cells, dominant-negative kinase mutants, NF-κB reporter assays, chemokine/cytokine expression analysis Immunity High 12387745
2002 NIK and IKKα mediate LTBR-induced NF-κB activation through phosphorylation of the p65 subunit at serine 536 in its transactivation domain 1 (TA1); this phosphorylation is required for transcriptional activation without altering IκB phosphorylation levels or p65 nuclear localization, revealing a distinct mechanism for LTBR-driven NF-κB activity. Dominant-negative kinase mutants (NIK, IKKα), Gal4-fusion transactivation reporter assay, site-directed mutagenesis of p65-Ser536, phosphorylation detection following LTbetaR stimulation The Journal of biological chemistry High 12419817
2006 LTBR signaling controls the development and maintenance of tertiary lymphoid organs (TLO) in the pancreas; blockade of TNFSF14 (LIGHT) signaling reduces LTBR-controlled migration factor expression and disrupts TLO organization, preventing diabetes in NOD mice; transgenic TNFSF14 expression in islets rapidly promotes TLO formation even without draining lymph nodes. In vivo blockade of TNFSF14, transgenic mouse model, gene expression analysis, histology Immunity High 16934497
2009 Hepatic LT-alpha/LT-beta overexpression drives liver inflammation and HCC in mice; HCC development depends on lymphocytes and hepatocyte IKKβ but not TNFR1; in vivo LTbetaR stimulation implicates hepatocytes as the major LT-responsive liver cells; LTbetaR inhibition suppresses HCC formation in LT-transgenic mice with hepatitis. Liver-specific LTalphabeta transgenic mouse model, genetic knockout (IKKβ, TNFR1), in vivo LTbetaR blocking, histopathology Cancer cell High 19800575
2016 LIGHT activates LTBR signaling in tumors, leading to production of chemokines that recruit T cells; antibody-guided tumor targeting of LIGHT creates a T cell-inflamed microenvironment and overcomes resistance to PD-L1 checkpoint blockade, establishing LTBR signaling as a driver of T cell infiltration and anti-tumor immunity. Antibody-LIGHT fusion protein, in vivo tumor models, T cell infiltration analysis, combination immunotherapy Cancer cell High 26977880
2020 LTbetaR signaling promotes non-canonical NF-κB activation and TGFβ signaling in lung epithelial cells, driving COPD pathology; therapeutic inhibition of LTbetaR disrupts inducible bronchus-associated lymphoid tissue (iBALT), prevents epithelial cell death, activates WNT/β-catenin signaling in alveolar epithelial progenitor cells, and induces lung tissue regeneration and reversion of airway fibrosis in mice. In vivo LTbetaR blocking in mouse models (young and aged, cigarette smoke-exposed), signaling pathway analysis, cell death assays, WNT reporter assays, patient tissue analysis Nature High 33149305
2022 CREB1 transcriptionally activates LTBR expression in lung epithelial cells; LTBR mediates NF-κB pathway activation downstream of hyperoxia; silencing LTBR rescues hyperoxia-induced suppression of cell viability and promotion of apoptosis in A549 and ATII cells, establishing a CREB1/LTBR/NF-κB axis in bronchopulmonary dysplasia. Luciferase reporter assay, ChIP assay, siRNA knockdown, cell viability assay (CCK-8), flow cytometry apoptosis assay Computational and mathematical methods in medicine Medium 36118831
2023 TRAF5 interacts with LTBR in HCC cells (confirmed by co-immunoprecipitation and immunofluorescence); TRAF5 silencing downregulates LTBR expression and suppresses LTBR-mediated NF-κB signaling, enhancing necroptosis (phosphorylation of RIP1 and MLKL); LTBR overexpression rescues the pro-necroptotic and anti-proliferative effects of TRAF5 knockdown. Co-immunoprecipitation, immunofluorescence, siRNA knockdown, overexpression rescue, western blotting, xenograft model PeerJ Medium 37366426
2024 LTBR maintains immunosuppressive M2 phenotype of tumor-associated macrophages (TAMs) through non-canonical NF-κB and Wnt/β-catenin signaling pathways; macrophage-specific knockout of LTBR hinders tumor growth and prolongs survival in vivo by blocking TAM immunosuppressive activity; TAM-targeted LTBR siRNA delivery improves ICI therapeutic response. Macrophage-specific conditional knockout, siRNA delivery, in vivo tumor models, signaling pathway analysis, immunofluorescence, single-cell RNA-seq analysis iMeta Medium 39429877
2024 Lymphotoxin-beta (LTβ) ligand activates the LTBR/NIK/RelB non-canonical NF-κB axis in cholangiocarcinoma cells, promoting proliferation; NIK inhibitor B022 suppresses RelB expression in patient-derived CCA organoids and blocks nuclear co-translocation of RelB and p52 stimulated by LTα1/β2. LTα1/β2 stimulation, NIK small-molecule inhibitor, patient-derived organoids, real-time impedance measurement, immunoblot, RNA sequencing, in vivo murine CCA models Liver international Medium 39164890
2013 Recombinant rabbit TNFSF14 (OcsTNFSF14) and extracellular LTBR (OceLTBR) proteins bind splenic T cells in vitro, confirming that the TNFSF14-LTBR ligand-receptor interaction is conserved in Oryctolagus cuniculus. Recombinant protein expression, confocal laser microscopy binding assay, SDS-PAGE, Western blot Molecular immunology Low 23370464
2026 FAP-targeted LTBR agonist (FAP-LTBR) selectively activates endothelial cells via LTBR signaling in a FAP-dependent manner, inducing chemokine secretion, T cell adhesion and extravasation, HEV differentiation, TLS-like immune aggregate formation, and increased B and T cell (including stem-like TCF1+ CD8+) infiltration in murine tumor models. FAP-LTBR bispecific agonist, primary human endothelial cells, 3D microfluidic vascular models, multiple murine tumor models, spatial transcriptomics, 3D immunophenotyping Clinical cancer research Medium 42012453
2025 LTβR and IFN sensing pathways are necessary and sufficient for HLA class I-independent cancer cell lysis by CD8+ TIL; whole-genome CRISPR loss-of-function screen nominated LTBR as a key determinant of TIL-mediated killing; expanded CD8+ TIL express high LTB and upregulate LTA upon co-culture with cancer cells. Whole-genome CRISPR loss-of-function screen, patient-derived TIL-melanoma co-cultures, scRNA-seq, scTCR-seq, validation knockouts bioRxivpreprint Medium

Source papers

Stage 0 corpus · 40 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
2015 The BioPlex Network: A Systematic Exploration of the Human Interactome. Cell 1118 26186194
2017 Architecture of the human interactome defines protein communities and disease networks. Nature 1085 28514442
2015 A human interactome in three quantitative dimensions organized by stoichiometries and abundances. Cell 1015 26496610
1995 The Epstein-Barr virus transforming protein LMP1 engages signaling proteins for the tumor necrosis factor receptor family. Cell 885 7859281
2020 A reference map of the human binary protein interactome. Nature 849 32296183
2002 The lymphotoxin-beta receptor induces different patterns of gene expression via two NF-kappaB pathways. Immunity 761 12387745
2003 Complete sequencing and characterization of 21,243 full-length human cDNAs. Nature genetics 754 14702039
2021 Dual proteome-scale networks reveal cell-specific remodeling of the human interactome. Cell 705 33961781
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
1998 LIGHT, a new member of the TNF superfamily, and lymphotoxin alpha are ligands for herpesvirus entry mediator. Immunity 618 9462508
2021 Multilevel proteomics reveals host perturbations by SARS-CoV-2 and SARS-CoV. Nature 532 33845483
2004 The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). Genome research 438 15489334
2005 Diversification of transcriptional modulation: large-scale identification and characterization of putative alternative promoters of human genes. Genome research 409 16344560
1994 A lymphotoxin-beta-specific receptor. Science (New York, N.Y.) 342 8171323
2003 Large-scale identification and characterization of human genes that activate NF-kappaB and MAPK signaling pathways. Oncogene 331 12761501
2009 A lymphotoxin-driven pathway to hepatocellular carcinoma. Cancer cell 329 19800575
2016 Facilitating T Cell Infiltration in Tumor Microenvironment Overcomes Resistance to PD-L1 Blockade. Cancer cell 321 26977880
1999 A newly identified member of tumor necrosis factor receptor superfamily (TR6) suppresses LIGHT-mediated apoptosis. The Journal of biological chemistry 304 10318773
1996 TRAF5, an activator of NF-kappaB and putative signal transducer for the lymphotoxin-beta receptor. The Journal of biological chemistry 304 8663299
2017 Genome-wide CRISPR screen identifies HNRNPL as a prostate cancer dependency regulating RNA splicing. Proceedings of the National Academy of Sciences of the United States of America 282 28611215
1997 Herpesvirus entry mediator, a member of the tumor necrosis factor receptor (TNFR) family, interacts with members of the TNFR-associated factor family and activates the transcription factors NF-kappaB and AP-1. The Journal of biological chemistry 256 9162022
2005 Muscle atrophy and bone loss after 90 days' bed rest and the effects of flywheel resistive exercise and pamidronate: results from the LTBR study. Bone 219 15811637
2011 Toward an understanding of the protein interaction network of the human liver. Molecular systems biology 207 21988832
1997 Hepatitis C virus core protein interacts with the cytoplasmic tail of lymphotoxin-beta receptor. Journal of virology 188 8995654
2000 The lymphotoxin-beta receptor is necessary and sufficient for LIGHT-mediated apoptosis of tumor cells. The Journal of biological chemistry 178 10799510
2001 A diverse family of proteins containing tumor necrosis factor receptor-associated factor domains. The Journal of biological chemistry 176 11279055
1997 Lymphotoxin-beta receptor signaling complex: role of tumor necrosis factor receptor-associated factor 3 recruitment in cell death and activation of nuclear factor kappaB. Proceedings of the National Academy of Sciences of the United States of America 157 9122217
2002 The NF-kappa B activation in lymphotoxin beta receptor signaling depends on the phosphorylation of p65 at serine 536. The Journal of biological chemistry 154 12419817
2006 Recruitment and activation of naive T cells in the islets by lymphotoxin beta receptor-dependent tertiary lymphoid structure. Immunity 148 16934497
2020 Inhibition of LTβR signalling activates WNT-induced regeneration in lung. Nature 141 33149305
2007 The IclR-type transcriptional repressor LtbR regulates the expression of leucine and tryptophan biosynthesis genes in the amino acid producer Corynebacterium glutamicum. Journal of bacteriology 42 17259312
2024 LTBR acts as a novel immune checkpoint of tumor-associated macrophages for cancer immunotherapy. iMeta 13 39429877
2022 CREB1 Transcriptionally Activates LTBR to Promote the NF-κB Pathway and Apoptosis in Lung Epithelial Cells. Computational and mathematical methods in medicine 9 36118831
2017 Association of LTBR polymorphisms with chronic hepatitis B virus infection and hepatitis B virus-related hepatocellular carcinoma. International immunopharmacology 8 28575727
2024 Lymphotoxin beta-activated LTBR/NIK/RELB axis drives proliferation in cholangiocarcinoma. Liver international : official journal of the International Association for the Study of the Liver 7 39164890
2023 Silencing of TRAF5 enhances necroptosis in hepatocellular carcinoma by inhibiting LTBR-mediated NF-κB signaling. PeerJ 6 37366426
2024 Comprehensive analysis reveals that LTBR is a immune-related biomarker for glioma. Computers in biology and medicine 4 38599071
2013 Molecular characterization, expression and binding activity of the cytokines TNFSF14 and its receptor LTBR in Oryctolagus cuniculus (rabbit). Molecular immunology 3 23370464
2026 FAP-Targeted LTBR Agonist Drives HEV Differentiation and Immune Niche Formation for Improved Immunotherapy Response in Solid Tumours. Clinical cancer research : an official journal of the American Association for Cancer Research 0 42012453