High Expression of IL-36γ in Influenza Patients Regulates Interferon Signaling Pathway and Causes Programmed Cell Death During Influenza Virus Infection

Liu, Shuai; Li, Hui; Wang, Yeming; Li, Haibo; Du, Sisi; Zou, Xiaohui; Zhang, Xulong; Cao, Bin

doi:10.3389/fimmu.2020.552606

Cited by 12 publications

(8 citation statements)

References 47 publications

(55 reference statements)

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“…In the mouse model of influenza virus-induced pneumonia, IL-36R deficiency mitigates mortality and lung damage, which is correlated to the reduction in the levels of pro-inflammatory factors, chemokines, and neutrophil aggregation ( 62 ). In addition, high IL-36γ expression levels promote the apoptosis of influenza A virus-infected lung epithelial cells, inhibit autophagy, and interfere with the IFN signaling pathway in vivo ( 63 ). IL-36γ is an important homeostatic regulator in antiviral response and viral immune evasion ( 63 ).…”

Section: Il-36 Cytokines and Inflammationmentioning

confidence: 99%

“…In addition, high IL-36γ expression levels promote the apoptosis of influenza A virus-infected lung epithelial cells, inhibit autophagy, and interfere with the IFN signaling pathway in vivo ( 63 ). IL-36γ is an important homeostatic regulator in antiviral response and viral immune evasion ( 63 ). The IL-36γ expression in airway epithelial cells can be enhanced by rhinovirus infection in asthmatic patients ( 64 ).…”

Section: Il-36 Cytokines and Inflammationmentioning

confidence: 99%

“…Furthermore, IL-36γ can induce autophagy in cells infected with Mycobacterium tuberculosis , and enhance the bacterial clearance ( 59 ). Interestingly, IL-36γ promotes lung epithelial cell apoptosis and attenuates autophagy following influenza A virus infection, and enhances the antiviral immune response ( 63 ). Accumulating evidence has implicated autophagy in the pathogenesis of airway inflammation and airway remodeling in asthma ( 67 , 78 , 79 ).…”

Section: Il-36 Cytokines and Autophagymentioning

confidence: 99%

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IL-36 Cytokines: Their Roles in Asthma and Potential as a Therapeutic

Dong

Hao

et al. 2022

Front. Immunol.

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Interleukin (IL)-36 cytokines are members of the IL-1 superfamily, which consists of three agonists (IL-36α, IL-36β and IL-36γ) and an IL-36 receptor antagonist (IL-36Ra). IL-36 cytokines are crucial for immune and inflammatory responses. Abnormal levels of IL-36 cytokine expression are involved in the pathogenesis of inflammation, autoimmunity, allergy and cancer. The present study provides a summary of recent reports on IL-36 cytokines that participate in the pathogenesis of inflammatory diseases, and the potential mechanisms underlying their roles in asthma. Abnormal levels of IL-36 cytokines are associated with the pathogenesis of different types of asthma through the regulation of the functions of different types of cells. Considering the important role of IL-36 cytokines in asthma, these may become a potential therapeutic target for asthma treatment. However, existing evidence is insufficient to fully elucidate the specific mechanism underlying the action of IL-36 cytokines during the pathological process of asthma. The possible mechanisms and functions of IL-36 cytokines in different types of asthma require further studies.

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Section: Il-36 Cytokines and Inflammationmentioning

confidence: 99%

Section: Il-36 Cytokines and Inflammationmentioning

confidence: 99%

Section: Il-36 Cytokines and Autophagymentioning

confidence: 99%

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IL-36 Cytokines: Their Roles in Asthma and Potential as a Therapeutic

Dong

Hao

et al. 2022

Front. Immunol.

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“…Although IAV induced complete autophagy to degrade antiviral factors for viral replication by IAV PB1-F2 protein[ 72 ], host IL-36γ limited autophagy to upregulate antiviral immunity for blocking IAV replication in the early stages of IAV infection[ 76 ]. Heat shock protein 70 inhibited the activity of IAV ribonucleoprotein, the interaction between IAV M1 protein and vRNP and blocked the replication of IAV [ 77 , 78 ].…”

Section: Host Regulates Autophagic Machinery Against Influenza Virus ...mentioning

confidence: 99%

The battle for autophagy between host and influenza A virus

et al. 2021

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Influenza A virus (IAV) is an infectious pathogen, threatening the population and public safety with its epidemics. Therefore, it is essential to better understand influenza virus biology to develop efficient strategies against its pathogenicity. Autophagy is an important cellular process to maintain cellular homeostasis by cleaning up the hazardous substrates in lysosome. Accumulating research has also suggested that autophagy is a critical mechanism in host defense responses against IAV infection by degrading viral particles and activating innate or acquired immunity to induce viral clearance. However, IAV has conversely hijacked autophagy to strengthen virus infection by blocking autophagy maturation and further interfering host antiviral signalling to promote viral replication. Therefore, how the battle for autophagy between host and IAV is carried out need to be known. In this review, we describe the role of autophagy in host defence and IAV survival, and summarize the role of influenza proteins in subverting the autophagic process as well as then concentrate on how host utilize antiviral function of autophagy to prevent IAV infection.

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“…Numerous studies have described the critical importance of IL‐36γ in host defense against lung infections caused by various pathogenic bacteria 6 . IL‐36γ expression was discovered to be aberrant in numerous inflammatory and autoimmune disorders such as rheumatoid arthritis (RA), 7 systemic lupus erythematosus (SLE), 8 psoriasis, 9 chronic obstructive pulmonary disease (COPD), 10,11 and acute respiratory distress syndrome (ARDS) 12 . Recent studies also found that IL‐36γ play a key role in type 2 diabetes mellitus (T2DM), which is related to chronic inflammation 13 .…”

Section: Introductionmentioning

confidence: 99%

A novel biomarker for pleural effusion diagnosis: Interleukin‐36γ in pleural fluid

Guo

Zhang

et al. 2022

Clinical Laboratory Analysis

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Background Numerous studies have described the critical importance of interleukin (IL) ‐36γ in host defense against lung infections, but it is unknown whether it plays a role in infectious pleural effusion (IPE). This study aimed to examine the levels of IL‐36γ in pleural effusions of different etiologies and evaluate the diagnostic accuracy of IL‐36γ in the differential diagnosis of IPE. Methods A total of 112 individuals was enrolled in this research. IL‐36γ levels in pleural fluids of all 112 patients were measured by enzyme‐linked immunosorbent assay (ELISA). We also characterized these markers' diagnostic values across various groups. Results Patients with tuberculous pleural effusion (TPE) and parapneumonic effusion (PPE) had exhibited markedly higher IL‐36γ levels in their pleural fluid than the malignant pleural effusion (MPE) and transudative effusion patients. Furthermore, the IL‐36γ concentrations in TPE patients were evidently higher than in uncomplicated parapneumonic effusion (UPPE) patients but significantly lower than in complicated parapneumonic effusion (CPPE)/empyema patients. Pleural fluid IL‐36γ is a useful marker to differentiate TPE from UPPE, at a cut‐off value for 657.5 pg/ml (area under the curve = 0.904, p < 0.0001) with 70.0% sensitivity and 95.7% specificity. Conclusions The elevated IL‐36γ in pleural effusion may be used as a novel biomarker for infectious pleural effusion diagnosis, particularly in patients with CPPE/empyema, and is a potentially promising biomarker to differentiate between TPE and UPPE.

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High Expression of IL-36γ in Influenza Patients Regulates Interferon Signaling Pathway and Causes Programmed Cell Death During Influenza Virus Infection

Cited by 12 publications

References 47 publications

IL-36 Cytokines: Their Roles in Asthma and Potential as a Therapeutic

IL-36 Cytokines: Their Roles in Asthma and Potential as a Therapeutic

The battle for autophagy between host and influenza A virus

A novel biomarker for pleural effusion diagnosis: Interleukin‐36γ in pleural fluid

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