Hvem

Shui, Jr-Wen; Kronenberg, Mitchell

doi:10.4161/gmic.23443

Cited by 22 publications

(19 citation statements)

References 58 publications

(79 reference statements)

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“… 12 , 13 Furthermore, the BTLA/HVEM pathway appears to be a new possible approach of immune escape and is considered to be a critical factor in the physiological process of inflammation and tumorigenesis. 14 , 15 …”

Section: Introductionmentioning

confidence: 99%

Increased BTLA and HVEM in gastric cancer are associated with progression and poor prognosis

Lan¹,

Li²,

Gao³

et al. 2017

OTT

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PurposeDeregulation of immune checkpoint molecules by tumor cells is related to immune escape. This study was conducted to investigate the relationship between the appearance of B- and T-lymphocyte attenuator (BTLA) and its ligand herpesvirus entry mediator (HVEM) with the prognosis in gastric cancer patients.Patients and methodsA total of 136 patients with curative gastrectomy were included. The expression of BTLA and HVEM was detected by immunohistochemistry, and its correlation with the clinical significance of gastric cancer was further analyzed.ResultsThe positivity of BTLA and HVEM was detected in 74.3% (101/136) and 89.0% (121/136) of the gastric cancer specimens, respectively. A high expression of BTLA and HVEM was detected, respectively, in 28.7% (39/136) and 44.9% (61/136) of the specimens. Characteristics analysis showed that the high expression of BTLA was significantly associated with lymph node metastasis (P=0.030). Similarly, the high expression of HVEM was also significantly correlated with lymph node metastasis (P=0.007) and depth of invasion (P=0.011). In addition, there was a positive correlation between the expression of BTLA and HVEM in gastric cancer specimens (r=0.245, P=0.004). Univariate analysis revealed that the high expression of BTLA and HVEM was associated with overall survival of patients along with tumor size, Borrmann type, depth of invasion, lymph node metastasis, and histological grade (P<0.05). Multivariate analysis established that the high expression of HVEM (P=0.010), depth of invasion (P=0.001), lymph node metastasis (P<0.001), and histological grade (P=0.027) were independent prognostic factors associated with overall survival in patients with gastric cancer.ConclusionThe increased BTLA and HVEM levels correlate with the development and poor prognosis of gastric cancer. HVEM is an important prognostic indicator, and BTLA/HVEM pathway is considered to be a promising candidate for immunotherapy of gastric cancer.

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Section: Introductionmentioning

confidence: 99%

Increased BTLA and HVEM in gastric cancer are associated with progression and poor prognosis

Lan¹,

Li²,

Gao³

et al. 2017

OTT

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“…Elegant studies of innate responses to bacteria in lung and gut mucosal epithelia have found a similar role for host HVEM signaling in the induction of IL-6 and other cytokines (22). In this model, CD160 on innate-like intraepithelial lymphocytes activates HVEM, which is highly expressed by the intestinal epithelium, resulting in NF-B-mediated Stat3 activation and increased expression of genes and peptides related to epithelial immunity (22,23). During HSK, the corneal epithelium secretes IL-6 and other cytokines in response to HSV-1 infection (91,92).…”

Section: Hvem Alters Host Immune Responses To Hsvmentioning

confidence: 99%

“…Outside of the eye, HVEM expression is broad: although its expression fluctuates throughout maturation, HVEM is found on most types of leukocytes, including T and B cells, dendritic cells (DCs), natural killer (NK) cells, and myeloid cells (56). HVEM is also highly expressed by nervous tissue and gut and lung epithelia (23,57).…”

Section: Hvem Alters Host Immune Responses To Hsvmentioning

confidence: 99%

“…However, HSK is an inflammatory disease, brought about by host infiltrates, particularly CD4 ϩ T cells and polymorphonuclear cells (PMN), that invade the murine cornea several days after replicating virus has been cleared and that persist chronically (14)(15)(16)(17)(18). A dizzying array of cytokines, chemokines, and immune cell types have been implicated in the pathogenesis of HSK, the temporal and functional relationships of which have been expertly reviewed elsewhere (11,15,(18)(19)(20) (21)(22)(23)(24)(25) and has been found to influence HSV pathogenesis in the murine eye during most stages of infection, including entry/acute viral replication, early/innate responses, chronic inflammation, and even viral latency. Results from our laboratory indicate that HVEM functions as a proinflammatory factor in murine herpes keratitis and call into question its importance as an entry receptor during ocular infection.…”

mentioning

confidence: 99%

“…Here, we focus on a single host factor, herpesvirus entry mediator (HVEM, also called tumor necrosis factor [TNF] superfamily member receptor 14 [Tnfrsf14]), originally identified as a viral entry receptor. HVEM has a multitude of roles in mucosal responses to a variety of pathogens (21)(22)(23)(24)(25) and has been found to influence HSV pathogenesis in the murine eye during most stages of infection, including entry/acute viral replication, early/innate responses, chronic inflammation, and even viral latency. Results from our laboratory indicate that HVEM functions as a proinflammatory factor in murine herpes keratitis and call into question its importance as an entry receptor during ocular infection.…”

mentioning

confidence: 99%

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Herpesvirus Entry Mediator and Ocular Herpesvirus Infection: More than Meets the Eye

Edwards

Longnecker

2017

J Virol

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As its name suggests, the host receptor herpesvirus entry mediator (HVEM) facilitates herpes simplex virus (HSV) entry through interactions with a viral envelope glycoprotein. HVEM also bridges several signaling networks, binding ligands from both tumor necrosis factor (TNF) and immunoglobulin (Ig) superfamilies with diverse, and often opposing, outcomes. While HVEM was first identified as a viral entry receptor for HSV, it is only recently that HVEM has emerged as an important host factor in immunopathogenesis of ocular HSV type 1 (HSV-1) infection. Surprisingly, HVEM exacerbates disease development in the eye independently of entry. HVEM signaling has been shown to play a variety of roles in modulating immune responses to HSV and other pathogens, and there is increasing evidence that these effects are responsible for HVEM-mediated pathogenesis in the eye. Here, we review the dual branches of HVEM function during HSV infection: entry and immunomodulation. HVEM is broadly expressed; intersects two important immunologic signaling networks; and impacts autoimmunity, infection, and inflammation. We hope that by understanding the complex range of effects mediated by this receptor, we can offer insights applicable to a wide variety of disease states.KEYWORDS HVEM, herpes simplex virus, herpes stromal keratitis H erpes simplex virus 1 (HSV-1) infects the majority of the world's population by adulthood and is responsible for the vast majority of ocular herpesvirus infections (1-3). In humans and mice, HSV-1 establishes lifelong latency in the trigeminal ganglia (TG) (4,5). Reactivations of HSV-1 in the TG can lead to anterograde movement of the virus along the ophthalmic branch of the trigeminal nerve, resulting in recurrent infection of virtually all the superficial tissues of the eye, including the cornea, conjunctiva, and eyelid (6-8). Ocular herpesvirus infections can lead to epithelial ulceration of the cornea, uveitis, and retinitis but most commonly cause herpes stromal keratitis, or HSK (9). HSK is characterized by chronic inflammation of the corneal stroma, leading to corneal thickening, opacification, scarring, and, potentially, blindness (10, 11). While reactivation accounts for the majority of human disease, most murine studies of HSK model primary infection as mice do not efficiently or reliably reactivate from latency (6).In the primary murine model of HSK, actively replicating HSV-1 in the cornea is detectable by plaque assay for up to 5 to 6 days postinfection (dpi) (9,12). Viral replication initiates HSK, as UV-inactivated or replication-deficient mutant HSV fail to induce HSK in BALB/c mice (13). However, HSK is an inflammatory disease, brought about by host infiltrates, particularly CD4 ϩ T cells and polymorphonuclear cells (PMN), that invade the murine cornea several days after replicating virus has been cleared and that persist chronically (14)(15)(16)(17)(18). A dizzying array of cytokines, chemokines, and immune cell types have been implicated in the pathogenesis of HSK, the temporal and...

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The co-inhibitory pathway and cellular immune imbalance in the progress of HBV infection

Chen

Wang

et al. 2013

Hepatol Int

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Co-inhibitory molecules play more important roles than co-stimulatory molecules. Increased PD-1 and BTLA/HVEM inhibited immune cells and the immune process. At the same time activated Stat3 and Stat5 stimulate the key factors in differentiation of Th17 and Treg, thus leading to imbalanced expansion of Th17 and Treg; immune tolerance was induced and HBV persistent. This resulted in hepatic inflammation that progressed to cirrhosis and carcinoma.

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Hvem

Cited by 22 publications

References 58 publications

Increased BTLA and HVEM in gastric cancer are associated with progression and poor prognosis

Increased BTLA and HVEM in gastric cancer are associated with progression and poor prognosis

Herpesvirus Entry Mediator and Ocular Herpesvirus Infection: More than Meets the Eye

The co-inhibitory pathway and cellular immune imbalance in the progress of HBV infection

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