ArticleThe Journal of experimental medicine2011
Herpesvirus entry mediator (TNFRSF14) regulates the persistence of T helper memory cell populations.
Article in The Journal of experimental medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
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Who cites it
48 citing papers in PubMed, 76 citations in OpenAlex.
- Complete disruption of gD binding to HVEM alters virus replication and host receptor homeostasis.PLoS pathogens · 2026Article
- LIGHT in combination with IL-13 or IL-17 drives inflammatory transcriptional signatures in human pulmonary fibroblasts relevant for human lung disease.ImmunoHorizons · 2025Article
- Intrathecal Inflammatory Profile and Gray Matter Damage Predict Progression Independent of Relapse Activity in Early Multiple Sclerosis.Neurology(R) neuroimmunology & neuroinflammation · 2025Article
- Internal regulation between constitutively expressed T cell co-inhibitory receptors BTLA and CD5 and tolerance in recent thymic emigrants.Open biology · 2024Article
- LIGHT/TNFSF14 promotes CAR-T cell trafficking and cytotoxicity through reversing immunosuppressive tumor microenvironment.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Beyond the anti-PD-1/PD-L1 era: promising role of the BTLA/HVEM axis as a future target for cancer immunotherapy.Molecular cancer · 2023Review
- TNFSF14/LIGHT promotes cardiac fibrosis and atrial fibrillation vulnerability via PI3Kγ/SGK1 pathway-dependent M2 macrophage polarisation.Journal of translational medicine · 2023Article
- Genetic deletion of HVEM in a leukemia B cell line promotes a preferential increase of PD-1Frontiers in immunology · 2023Article
- T cell co-stimulatory and co-inhibitory pathways in atopic dermatitis.Frontiers in immunology · 2023Review
- A Deficiency in the Cytokine TNFSF14/LIGHT Limits Inflammation and Remodeling in Murine Eosinophilic Esophagitis.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Realigning the LIGHT signaling network to control dysregulated inflammation.The Journal of experimental medicine · 2022Article
- CD137 as an Attractive T Cell Co-Stimulatory Target in the TNFRSF for Immuno-Oncology Drug Development.Cancers · 2021Review
- Article
- Single-Cell Transcriptomic Analysis Reveals BCMA CAR-T Cell Dynamics in a Patient with Refractory Primary Plasma Cell Leukemia.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Single-Cell RNA Sequencing Reveals Tissue Compartment-Specific Plasticity of Mycosis Fungoides Tumor Cells.Frontiers in immunology · 2021Article
- Differential Expression of Circulating Inflammatory Proteins Following Sport-Related Traumatic Brain Injury.International journal of molecular sciences · 2020Article
- Accelerator or Brake: Immune Regulators in Malaria.Frontiers in cellular and infection microbiology · 2020Review
- Article
- Redirection to the bone marrow improves T cell persistence and antitumor functions.The Journal of clinical investigation · 2018Article
- HVEM and CD160: Regulators of Immunopathology During Malaria Blood-Stage.Frontiers in immunology · 2018Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Memory T helper cells (Th cells) play an important role in host defense against pathogens but also contribute to the pathogenesis of inflammatory disorders. We found that a soluble decoy lymphotoxin β receptor (LT-βR)-Fc, which can block tumor necrosis factor (TNF)-related ligands LIGHT (TNFSF14) and LT-αβ binding to the herpesvirus entry mediator (HVEM) and the LT-βR, inhibited the accumulation of memory Th2 cells after antigen encounter and correspondingly reduced inflammatory responses in vivo. Showing that this was a function of the receptor for LIGHT, antigen-specific memory CD4 T cells deficient in HVEM were also unable to persist, despite having a normal immediate response to recall antigen. HVEM(-/-) memory Th2 cells displayed reduced activity of PKB (protein kinase B; Akt), and constitutively active Akt rescued their survival and restored strong inflammation after antigen rechallenge. This was not restricted to Th2 memory cells as HVEM-deficient Th1 memory cells were also impaired in surviving after encounter with recall antigen. Furthermore, the absence of LIGHT on T cells recapitulated the defect seen with the absence of HVEM, suggesting that activated T cells communicate through LIGHT-HVEM interactions. Collectively, our results demonstrate a critical role of HVEM signals in the persistence of large pools of memory CD4 T cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.