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these results provide new insights into the tumor suppressor function of HVEM by elucidating the BTLA (show BTLA ELISA Kits)-dependent mechanism by which HVEM inhibits BCR (show BCR ELISA Kits) signaling and activation of the tumor microenvironment, and provide evidence that immune cells can be engineered for the local delivery of anticancer therapies.
Low HVEM expression is associated with pancreatic and ampullary cancer.
HIV-1 produced from CD4 (show CD4 ELISA Kits)+ T cells bears HSV-2 receptor HVEM and can bind to and enter HSV-2-infected epithelial cells depending on HVEM-gD interaction and the presence of gB/gH/gL.
HVEM is highly expressed in ovarian serous adenocarcinoma tissues and correlated with the patient clinicopathological features.
TNFRSF14 and MAP2K1 (show MAP2K1 ELISA Kits) mutations are the most frequent genetic alterations found in pediatric-type follicular lymphoma (PTFL) and occur independently in most cases, suggesting that both mutations might play an important role in PTFL lymphomagenesis.
genetic landscape of Pediatric-type follicular lymphoma suggests that TNFRSF14 mutations accompanied by copy-number neutral loss of heterozygosity of the 1p36 locus in over 70% of mutated cases, as additional selection mechanism, might play a key role in the pathogenesis of this disease.
The increased immune-stimulatory capacity of lymphoma B cells with TNFRSF14 aberrations had clinical relevance, associating with higher incidence of acute GVHD in patients undergoing allogeneic hematopoietic stem cell transplantation.
These results suggest that TNFRSF14 mutations point towards a diagnosis of follicular lymphomas , and can be used in the sometimes difficult distinction between marginal zone lymphomas and follicular lymphomas
the overexpression of HVEM in ovarian cancer cells may suppress the proliferation and immune function of T cells, thus leading to the development of ovarian cancer. The current study partially explains the immune escape mechanism of ovarian cancer cells.
In eight cases (42%) we observed recurrent copy number loss of chr1:2,352,236-4,574,271, a region containing the candidate tumor suppressor TNFRSF14.
HVEM represents a critical signal for memory precursor effector cells and development of protective mucosal CD8 (show CD8A ELISA Kits) T cell memory
Dendritic cells require BTLA (show BTLA ELISA Kits) and HVEM to actively adjust tolerizing T cell responses under steady-state conditions.
we identified herpes virus entry mediator as a functional receptor that mediates SALM5 (show LRFN5 ELISA Kits)'s suppressive function. Our findings reveal a molecular link between the neuronal system and the immune system, and provide potential therapeutic targets for the control of CNS diseases.
results have revealed a novel role of HVEM on the regulation of IFN-I and immunopathology during Listeria infection.
our studies revealed a novel function of the HVEM cosignaling molecule and its ligands in EAU pathogenesis through the induction of Th1 (show HAND1 ELISA Kits)- and Th17-type T cell responses
Together, these data indicate that HVEM contributes to ocular pathogenesis independently of entry and point to an immunomodulatory role for this protein specifically on radiation-resistant cells.
results demonstrate a role for both nectin-1 (show PVRL1 ELISA Kits) and HVEM as receptors and suggest a further receptor which appears much less efficient.
Authors show that CD4 (show CD4 ELISA Kits)(+) FoxP3 (show FOXP3 ELISA Kits)(+) Tregs up- regulate HVEM (herpes virus entry mediator), which is a binding site for major viral glycoprotein gD, following herpes simplex virus 1 infection.
results support a model whereby BTLA (show BTLA ELISA Kits) on innate leukocytes is triggered by HVEM and delivers negative signals into BTLA (show BTLA ELISA Kits)(+) cells, thereby interfering with the protective immune response to this intestinal parasite.
In summary, herpes simplex virus 1 entry into epidermis was shown to strongly depend on the presence of nectin-1 (show PVRL1 ELISA Kits), but the restricted presence of HVEM can potentially replace nectin-1 (show PVRL1 ELISA Kits) as a receptor.
The protein encoded by this gene is a member of the TNF-receptor superfamily. This receptor was identified as a cellular mediator of herpes simplex virus (HSV) entry. Binding of HSV viral envelope glycoprotein D (gD) to this receptor protein has been shown to be part of the viral entry mechanism. The cytoplasmic region of this receptor was found to bind to several TRAF family members, which may mediate the signal transduction pathways that activate the immune response.
tumor necrosis factor receptor superfamily member 14
, tumor necrosis factor receptor superfamily, member 14 (herpesvirus entry mediator)
, herpesvirus entry mediator A
, CD40-like protein
, herpes virus entry mediator A
, tumor necrosis factor receptor-like 2
, tumor necrosis factor receptor-like gene2
, herpes virus entry mediator