Molecular cloning and characterization of TNFSF14 (LIGHT) and its receptor TNFRSF14 (HVEM) in guinea pig (Cavia porcellus)

Li, Chunlan; Chen, Shanshan; Song, Jiuzhou; Liu, Hongyan; Gu, Wei; Ai, Hongxin; Zhao, Bo; Zhang, Shuangquan

doi:10.1016/j.gene.2013.05.031

Cited by 3 publications

(3 citation statements)

References 46 publications

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“…7B). The expression pattern was consistent with those of other teleost LIGHT (25,80,81) and mammalian LIGHT (45,73,82). Additionally, the expression pattern of fugu LIGHT was similar to that of fugu LTbR except in PBLKs.…”

Section: Cytoplasmic Traf Binding Domains Of Fish Ltbrsupporting

confidence: 81%

Original Ligand for LTβR Is LIGHT: Insight into Evolution of the LT/LTβR System

Maeda

Suetake

Odaka

et al. 2018

The Journal of Immunology

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The lymphotoxin (LT)/LTβ receptor (LTβR) axis is crucial for the regulation of immune responses and development of lymphoid tissues in mammals. Despite the importance of this pathway, the existence and function of LT and LTβR remain obscure for nonmammalian species. In this study, we report a nonmammalian LTβR and its ligand. We demonstrate that TNF-New (TNFN), which has been considered orthologous to mammalian LT, was expressed on the cell surface as a homomer in vitro. This different protein structure indicates that TNFN is not orthologous to mammalian LTα and LTβ. Additionally, we found that LTβR was conserved in teleosts, but the soluble form of recombinant fugu LTβR did not bind to membrane TNFN under the circumstance tested. Conversely, the LTβR recombinant bound to another ligand, LIGHT, similar to that of mammals. These findings indicate that teleost LTβR is originally a LIGHT receptor. In the cytoplasmic region of fugu LTβR, recombinant fugu LTβR bound to the adaptor protein TNFR-associated factor (TRAF) 2, but little to TRAF3. This difference suggests that teleost LTβR could potentially activate the classical NF-κB pathway with a novel binding domain, but would have little ability to activate an alternative one. Collectively, our results suggested that LIGHT was the original ligand for LTβR, and that the teleost immune system lacked the LT/LTβR pathway. Acquisition of the LT ligand and TRAF binding domain after lobe-finned fish may have facilitated the sophistication of the immune system and lymphoid tissues.

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Section: Cytoplasmic Traf Binding Domains Of Fish Ltbrsupporting

confidence: 81%

Original Ligand for LTβR Is LIGHT: Insight into Evolution of the LT/LTβR System

Maeda

Suetake

Odaka

et al. 2018

The Journal of Immunology

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“…The Ii chain associated with MHC Ⅱ a chains and b chains could be involved in immune escape by inhibiting the expression of MHC Ⅱ molecule and endogenous antigens (Zhou et al., 2016). LIGHT (lymphotoxin‐related inducible ligand that competes with herpes simplex virus glycoprotein D for herpesvirus entry mediator on T cells) is a member of the tumour necrosis factor ligand superfamily, which plays important roles in inflammatory and immune responses (Li et al., 2013). Constitutive expression of LIGHT results in T cell‐mediated inflammation that causes tissue destruction, whereas the absence of LIGHT leads to deficient T cell responses (Shaikh et al., 2001).…”

Section: Discussionmentioning

confidence: 99%

Transcriptome analysis of turbot (Scophthalmus maximus) head kidney and liver reveals immune mechanism in response to Vibrio anguillarum infection

Song

Dong

2022

Journal of Fish Diseases

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The diseases triggered by Vibrio anguillarum infection have created huge economic losses to the turbot (Scophthalmus maximus) farming industry. However, the immune mechanism of turbot to V. anguillarum infection has not been deeply investigated. To better understand the immune response of turbot to V. anguillarum infection, transcriptome analysis of the head kidney and liver of turbot was performed. A total of 15,948 and 11,494 differentially expressed genes (DEGs) were obtained from the turbot head kidney and liver, respectively. Transcriptome analysis revealed that the head kidney and liver of turbot have some differences in the gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis of the DEGs for the different functions of these two organs. Although there are many uncertain factors in this immune process, such as the occurrence of alternative splicing (AS) events and the differences in the protein structure of the DEGs, the NFκB signalling pathway, MKK‐dependent AP‐1 activation, JAK‐STAT signalling pathway, the signal transmission of MHC Ⅰ and a series of DEGs including HSP90 driving NLRP3 to produce inflammatory factors (IL‐1β, IL‐8, TNFα, etc.) were possible important immune response pathways for turbot to V. anguillarum infection. Overall, our research has conducted a preliminary exploration of the immune mechanism of turbot in response to V. anguillarum infection.

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“…Similarly, DcR3 promotes chemotaxis of the T cells through inhibiting LIGHT-HVEM interaction 43 . Nevertheless, DcR3 can ameliorate T-cell responses to antigens by neutralising LIGHT-HVEM association 15,44 . However, there are no reports on how DcR3, secreted by HCC cells, suppresses CD4 + T-cell proliferation and differentiation.…”

Section: Discussionmentioning

confidence: 99%

Role of TGFβ3-Smads-Sp1 axis in DcR3-mediated immune escape of hepatocellular carcinoma

Zhu

Liu

et al. 2019

Oncogenesis

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Hepatocellular carcinoma (HCC) is a leading cause of tumour-associated mortality worldwide, but no significant improvement in treating HCC has been reported with currently available systemic therapies. Immunotherapy represents a new frontier in tumour therapy. Therefore, the immunobiology of hepatocarcinoma has been under intensive investigation. Decoy receptor 3 (DcR3), a member of the tumour necrosis factor receptor (TNFR) superfamily, is an immune suppressor associated with tumourigenesis and cancer metastasis. However, little is known about the role of DcR3 in the immunobiology of hepatocarcinoma. In this study, we found that overexpression of DcR3 in HCC is mediated by the TGFβ3-Smad-Sp1 signalling pathway, which directly targets DcR3 promoter regions. Moreover, overexpression of DcR3 in HCC tissues is associated with tumour invasion and metastasis and significantly promotes the differentiation and secretion of Th2 and Treg cells while inhibiting the differentiation and secretion of Th1 cells. Conversely, knockdown of DcR3 expression in HCC significantly restored the immunity of CD4 + T cells. Inhibition of DcR3 expression may provide a novel immunotherapeutic approach to restoring immunity in HCC patients.

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Molecular cloning and characterization of TNFSF14 (LIGHT) and its receptor TNFRSF14 (HVEM) in guinea pig (Cavia porcellus)

Cited by 3 publications

References 46 publications

Original Ligand for LTβR Is LIGHT: Insight into Evolution of the LT/LTβR System

Original Ligand for LTβR Is LIGHT: Insight into Evolution of the LT/LTβR System

Transcriptome analysis of turbot (Scophthalmus maximus) head kidney and liver reveals immune mechanism in response to Vibrio anguillarum infection

Role of TGFβ3-Smads-Sp1 axis in DcR3-mediated immune escape of hepatocellular carcinoma

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