SOCS3 Promotes ALV-J Virus Replication via Inhibiting JAK2/STAT3 Phosphorylation During Infection

Mo, Guodong; Fu, Huali; Hu, Bowen; Zhang, Qihong; Xian, Mingjian; Zhang, Zihao; Li, Gang; Shi, Meiqing; Nie, Qinghua; Zhang, Xiquan

doi:10.3389/fcimb.2021.748795

Cited by 16 publications

(15 citation statements)

References 43 publications

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“…SOCS3 is a critical negative regulator of the inflammatory response via JAK2/STAT3 activation 20,21 . Therefore, we measured the SOCS3 protein levels using western blot and investigated whether OCE could regulate SOCS3 production.…”

Section: Resultsmentioning

confidence: 99%

Ohwia caudata extract relieves the IL‐17A‐induced inflammatory response of synoviocytes through modulation of SOCS3 and JAK2/STAT3 activation

Kuo

et al. 2023

Environmental Toxicology

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Fibroblast-like synoviocytes accumulation, proliferation and activation, and the subsequent inflammatory mediators production play a key role in the progression of rheumatoid arthritis (RA). It is well established that Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling triggers inflammation, and induces cytokine levels in RA. Ohwia caudata have long been used against many disorders. However, in RA, the effects of O. caudata have not been elucidated. In the current study, synoviocytes were used to evaluate the suppressive effects of O. caudate extract (OCE) on the pro-inflammatory cytokines production. In vitro, the underlying mechanisms by which OCE inhibits inflammatory response through regulation of suppressors of cytokine signaling 3 (SOCS3) and JAK2/STAT3 expression in IL-17A-treated HIG-82 synoviocytes were investigated. The results demonstrated that the proliferation of Tsung-Jung Ho and Chih-Yang Huang contributed equally to this work.

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Section: Resultsmentioning

confidence: 99%

Ohwia caudata extract relieves the IL‐17A‐induced inflammatory response of synoviocytes through modulation of SOCS3 and JAK2/STAT3 activation

Kuo

et al. 2023

Environmental Toxicology

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“…In previous studies, the JAK-STAT signaling pathway, closely related to leukemia and myeloid production, was activated after ALV infection [ 36 , 37 ]. Among the seven STATs with known functions, STAT3 plays a key role in the malignant transformation of cells.…”

Section: Resultsmentioning

confidence: 99%

A20 Enhances the Expression of the Proto-Oncogene C-Myc by Downregulating TRAF6 Ubiquitination after ALV-A Infection

Chen

Wang

Yang

et al. 2022

Viruses

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Hens infected with avian leukosis virus subgroup A (ALV-A) experience stunted growth, immunosuppression, and potentially, lymphoma development. According to past research, A20 can both promote and inhibit tumor growth. In this study, DF-1 cells were infected with ALV-A rHB2015012, and Gp85 expression was measured at various time points. A recombinant plasmid encoding the chicken A20 gene and short hairpin RNA targeting chicken A20 (A20-shRNA) was constructed and transfected into DF-1 cells to determine the effect on ALV-A replication. The potential signaling pathways of A20 were explored using bioinformatics prediction, co-immunoprecipitation, and other techniques. The results demonstrate that A20 and ALV-A promoted each other after ALV-A infection of DF-1 cells, upregulated A20, inhibited TRAF6 ubiquitination, and promoted STAT3 phosphorylation. The phosphorylated-STAT3 (p-STAT3) promoted the expression of proto-oncogene c-myc, which may lead to tumorigenesis. This study will help to further understand the tumorigenic process of ALV-A and provide a reference for preventing and controlling ALV.

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“…Thus, CIS may be an important factor that helps ALV-J evade the innate immune response in host. Similarly, it has recently been shown that ALV-J infection could inhibit the phosphorylation of the JAK2/STAT3 signaling pathway by upregulating the expression of SOCS3, which represses host innate immunity and facilitates viral replication ( 121 ). In addition to directly targeting negative regulators for interferon signal transduction pathways to achieve innate immune evasion, ALV-J can also suppress the expression of IFN by targeting host protein indirectly ( 122 , 123 ).…”

Section: Innate Immune Evasion By Avian Leukosis Virus (Alv)mentioning

confidence: 99%

Advances on Innate Immune Evasion by Avian Immunosuppressive Viruses

Wang

Zheng

2022

Front. Immunol.

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Innate immunity is not only the first line of host defense against pathogenic infection, but also the cornerstone of adaptive immune response. Upon pathogenic infection, pattern recognition receptors (PRRs) of host engage pathogen-associated molecular patterns (PAMPs) of pathogens, which initiates IFN production by activating interferon regulatory transcription factors (IRFs), nuclear factor-kappa B (NF-κB), and/or activating protein-1 (AP-1) signal transduction pathways in host cells. In order to replicate and survive, pathogens have evolved multiple strategies to evade host innate immune responses, including IFN-I signal transduction, autophagy, apoptosis, necrosis, inflammasome and/or metabolic pathways. Some avian viruses may not be highly pathogenic but they have evolved varied strategies to evade or suppress host immune response for survival, causing huge impacts on the poultry industry worldwide. In this review, we focus on the advances on innate immune evasion by several important avian immunosuppressive viruses (infectious bursal disease virus (IBDV), Marek’s disease virus (MDV), avian leukosis virus (ALV), etc.), especially their evasion of PRRs-mediated signal transduction pathways (IFN-I signal transduction pathway) and IFNAR-JAK-STAT signal pathways. A comprehensive understanding of the mechanism by which avian viruses evade or suppress host immune responses will be of help to the development of novel vaccines and therapeutic reagents for the prevention and control of infectious diseases in chickens.

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SOCS3 Promotes ALV-J Virus Replication via Inhibiting JAK2/STAT3 Phosphorylation During Infection

Cited by 16 publications

References 43 publications

Ohwia caudata extract relieves the IL‐17A‐induced inflammatory response of synoviocytes through modulation of SOCS3 and JAK2/STAT3 activation

Ohwia caudata extract relieves the IL‐17A‐induced inflammatory response of synoviocytes through modulation of SOCS3 and JAK2/STAT3 activation

A20 Enhances the Expression of the Proto-Oncogene C-Myc by Downregulating TRAF6 Ubiquitination after ALV-A Infection

Advances on Innate Immune Evasion by Avian Immunosuppressive Viruses

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