Cloning, identification of the two cytokine receptor family B subunits CRFB1 and CRFB5 from grass carp (Ctenopharyngodon idella)

Chen, Huarong; Wenqun, Liu; Wang, Binhua; Mao, Huiling; Sun, Zhicheng; Hou, Qunhao; Mi, Yichuan; Fan, Li; Hu, Chengyu

doi:10.1016/j.fsi.2015.04.009

Cited by 12 publications

(3 citation statements)

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“…It has been proven that CRFB5 is a homolog of IFNAR1, while CRFB1 and CRFB2 are homologs of IFNAR2, as proven by sequence analysis and correlation experiments [19]. Some studies have found that virus infection or poly I:C stimulation could induce CRFB5 expression in some teleost fishes, including orange-spotted grouper (Epinephelus coioides), Asian Arowana (Scleropages formosus), Nile tilapia (Oreochromis niloticus), and grass carp [14,15,17,18]. For example, poly I:C stimulation caused the up-regulation of CRFB5 in the liver of tilapia and Asian arowana [14,20], as well as in grass carp kidney cells (CIK cell) [15], which demonstrated that CRFB5 was involved in antiviral immune responses in fish [20].…”

Section: Introductionmentioning

confidence: 99%

“…In teleost, the first type I IFN receptor was identified in the pufferfish (Tetraodontidae) cytokine receptor family B (CRFB) gene, which shares commonality with the cluster of IFN receptor genes found in mammals [12,13]. Different types of CRFB genes have been characterized in teleost fishes, such as CRFB1 and CRFB5 in zebrafish (Danio rerio), Atlantic salmon (Salmo salar), and grass carp (Ctenopharyngodon idella), CRFB2 and CRFB5 in tilapia (Oreochromis mossambicus) [14][15][16], and CRFB13 and CRFB17 in Arapaima (Arapaima gigas) [17]. Protein structure analysis showed that two of the fibronectin type-3 (FN3) domains were conserved in fish CRFB5, whereas four FN3 domains were present in human IFNAR1 [18].…”

Section: Introductionmentioning

confidence: 99%

“…Some studies have found that virus infection or poly I:C stimulation could induce CRFB5 expression in some teleost fishes, including orange-spotted grouper (Epinephelus coioides), Asian Arowana (Scleropages formosus), Nile tilapia (Oreochromis niloticus), and grass carp [14,15,17,18]. For example, poly I:C stimulation caused the up-regulation of CRFB5 in the liver of tilapia and Asian arowana [14,20], as well as in grass carp kidney cells (CIK cell) [15], which demonstrated that CRFB5 was involved in antiviral immune responses in fish [20]. However, whether fish CRFB5 could be induced by pathogen infection and involved in host antibacterial immunity remains unclear.…”

Section: Introductionmentioning

confidence: 99%

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CRFB5a, a Subtype of Japanese Eel (Anguilla japonica) Type I IFN Receptor, Regulates Host Antiviral and Antimicrobial Functions through Activation of IRF3/IRF7 and LEAP2

Wang,

Lin,

Wang

et al. 2023

Animals

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IFNAR1, one of the type I IFN receptors, is crucial to mammalian host defense against viral invasion. However, largely unknown is the immunological role of the fish teleost protein IFNAR1, also known as CRFB5. We have successfully cloned the whole cDNA of the Japanese eel’s (Anguilla japonica) CRFB5a homolog, AjCRFB5a. The two fibronectin-3 domains and the transmembrane region (238–260 aa) of AjCRFB5a are normally present, and it shares a three-dimensional structure with zebrafish, Asian arowana, and humans. According to expression analyses, AjCRFB5a is highly expressed in all tissues found, particularly the liver and intestine. In vivo, Aeromonas hydrophila, LPS, and the viral mimic poly I:C all dramatically increased AjCRFB5a expression in the liver. Japanese eel liver cells were reported to express AjCRFB5a more strongly in vitro after being exposed to Aeromonas hydrophila or being stimulated with poly I: C. The membranes of Japanese eel liver cells contained EGFP-AjCRFB5a proteins, some of which were condensed, according to the results of fluorescence microscopy. Luciferase reporter assays showed that AjCRFB5a overexpression strongly increased the expression of immune-related genes in Japanese eel liver cells, such as IFN1, IFN2, IFN3, IFN4, IRF3, IRF5, and IRF7 of the type I IFN signaling pathway, as well as one of the essential antimicrobial peptides LEAP2, in addition to significantly inducing human IFN-promoter activities in HEK293 cells. Additionally, RNA interference (RNAi) data demonstrated that knocking down AjCRFB5a caused all eight of those genes to drastically lower their expression in Japanese eel liver cells, as well as to variable degrees in the kidney, spleen, liver, and intestine. Our findings together showed that AjCRFB5a participates in the host immune response to bacterial infection by inducing antimicrobial peptides mediated by LEAP2 and favorably modulates host antiviral immune responses by activating IRF3 and IRF7-driven type I IFN signaling pathways.

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