Cytokines predict virological response in chronic hepatitis B patients receiving peginterferon alfa-2a therapy

Fu, Wenkang; Cao, Jie; Mi, Ningning; Huang, Chongfei; Gao, Long; Zhang, Jin-Duo; Yue, Ping; Bai, Bing; Lin, Yanyan; Meng, Wenbo

doi:10.12998/wjcc.v8.i11.2255

Cited by 4 publications

(4 citation statements)

References 45 publications

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“…The results revealed that 10 cytokines were highly abundant in patient serum: IP-10, TGF-β1, CXCL9, G-CSF, TNF-α, IFN-γ, IL-8, IL-16, TGF-β2, and IL-27. Among them, G-CSF, 17 IFN-γ, 18 IL-8, 19 IP-10, 20 CXCL9, 21 and IL-16 22 were reported to be associated with PEG-IFN therapy, which was confirmed in the present study. However, IL-21, 23 , 24 which has attracted research interest in chronic hepatitis B infection, was hardly detected in the serum samples from our PEG-IFN treatment cohort.…”

Section: Discussionsupporting

confidence: 87%

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Expression Pattern of Cytokines in Patients with Chronic Hepatitis B Receiving PEGinterferon Therapy

Chen¹,

Hong²,

Li³

et al. 2023

IJGM

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Purpose Chronic hepatitis B virus (CHB) infection is a worldwide health problem. Polyethylene glycol (PEG)ylated interferon (PEG-IFN) is an available therapy for CHB that has antiviral and immunomodulatory effects. However, PEG-IFN therapy is limited by the fact that only a subset of patients show a sustained response, its severe side effects, and high cost. The aim of this study was to explore novel biomarkers for the early prediction of PEG-IFN treatment response and to uncover its underlying mechanism. Patients and Methods We enrolled 10 paired patients with Hepatitis B e antigen (HBeAg)-positive CHB who received PEG-IFN-α2a monotherapy. Patient serum samples were collected at 0, 4, 12, 24, and 48 weeks and serum samples were collected from eight healthy people as healthy controls. For confirmation, we enrolled 27 patients with HBeAg-positive CHB receiving PEG-IFN therapy and serum samples at 0 and 12 weeks were obtained. Serum samples were analyzed using Luminex technology. Results Among 27 assessed cytokines, 10 cytokines were identified to have high expression levels. Among them, six cytokines had significant differences in their levels between the patients with HBeAg-positive CHB and the healthy controls (P < 0.05). Potentially, treatment response could be predicted using the early time points of 4, 12, and 24 weeks. Moreover, after 12 weeks of PEG-IFN treatment, increased levels of pro-inflammatory cytokines and decreased levels of anti-inflammatory cytokines were observed. The fold change of IP-10 between 12 weeks and 0 weeks correlated with the decrease in ALT levels from 0 to 12 weeks (r = 0.2675, P = 0.0024). Conclusion In patients with CHB, we observed a certain pattern in the levels of cytokines during treatment with PEG-IFN, and the cytokine IP-10 might be a potential biomarker for treatment response.

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Section: Discussionsupporting

confidence: 87%

“…This observation was consistent with the fact that IP-10 could be a potential marker for the response to PEG-IFN therapy. 20 , 25 …”

Section: Discussionmentioning

confidence: 99%

Expression Pattern of Cytokines in Patients with Chronic Hepatitis B Receiving PEGinterferon Therapy

Chen¹,

Hong²,

Li³

et al. 2023

IJGM

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“…Moreover, HBxAg stimulates virus gene expression and replication and is crucial for the establishment and maintenance of chronic carrier state. Intrahepatic inflammatory reactions [ 16 , 17 , 18 ] lead to the induction of several suppressive pathways and subsequent recruitment of regulatory cells that drive functional demolition of T cells [ 19 , 20 , 21 , 22 , 23 ]. These cells start overexpressing inhibitory receptors [ 9 , 24 , 25 , 26 , 27 ] that further dampen their functional status causing immune exhaustion, resulting in viral persistence and further disease progression [ 28 ].…”

Section: Innate and Adaptive Immune Response Against Hbv Infectionmentioning

confidence: 99%

Immunopathology of Chronic Hepatitis B Infection: Role of Innate and Adaptive Immune Response in Disease Progression

Khanam

Chua

Kottilil

2021

IJMS

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More than 250 million people are living with chronic hepatitis B despite the availability of highly effective vaccines and oral antivirals. Although innate and adaptive immune cells play crucial roles in controlling hepatitis B virus (HBV) infection, they are also accountable for inflammation and subsequently cause liver pathologies. During the initial phase of HBV infection, innate immunity is triggered leading to antiviral cytokines production, followed by activation and intrahepatic recruitment of the adaptive immune system resulting in successful virus elimination. In chronic HBV infection, significant alterations in both innate and adaptive immunity including expansion of regulatory cells, overexpression of co-inhibitory receptors, presence of abundant inflammatory mediators, and modifications in immune cell derived exosome release and function occurs, which overpower antiviral response leading to persistent viral infection and subsequent immune pathologies associated with disease progression towards fibrosis, cirrhosis, and hepatocellular carcinoma. In this review, we discuss the current knowledge of innate and adaptive immune cells transformations that are associated with immunopathogenesis and disease outcome in CHB patients.

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“…For example, CCL17 was associated with the development of murine colitis, 70 endometriosis 71 and myocardial inflammation 11 . Increased CCL17 levels correlate with the virological response of patients with chronic hepatitis B 72 and CCL17 has been considered to be a potential therapeutic target in cardiac hypertrophy and fibrosis, as well as in many other types of fibrosis 46 . High levels of the chemokine are seen in patients with food‐induced anaphylaxis, 73 gastrointestinal food allergies 74 and childhood allergy development, 75 with elevated CCL17 serum levels reported to be a potential diagnostic biomarker for food protein–induced enterocolitis syndrome, which is a non‐immunoglobulin E–mediated gut allergic response 76 .…”

Section: Ccl17 Biologymentioning

confidence: 99%

CCL17/TARC in autoimmunity and inflammation—not just a T‐cell chemokine

et al. 2023

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Chemokine (C-C) ligand 17 (CCL17) was first identified as thymus-and activation-regulated chemokine when it was found to be constitutively expressed in the thymus and identified as a T-cell chemokine. This chemoattractant molecule has subsequently been found at elevated levels in a range of autoimmune and inflammatory diseases, as well as in cancer. CCL17 is a C-C chemokine receptor type 4 (CCR4) ligand, with chemokine (C-C) ligand 22 being the other major ligand and, as CCR4 is highly expressed on helper T cells, CCL17 can play a role in T-cell-driven diseases, usually considered to be via its chemotactic activity on T helper 2 cells; however, given that CCR4 is also expressed by other cell types and there is elevated expression of CCL17 in many diseases, a broader CCL17 biology is suggested. In this review, we summarize the biology of CCL17, its regulation and its potential contribution to the pathogenesis of various preclinical models. Reference is made, for example, to recent literature indicating a role for CCL17 in the control of pain as part of a granulocyte macrophage-colony-stimulating factor/CCL17 pathway in lymphocyte-independent models and thus not as a T-cell chemokine. The review also discusses the potential for CCL17 to be a biomarker and a therapeutic target in human disorders.

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Cytokines predict virological response in chronic hepatitis B patients receiving peginterferon alfa-2a therapy

Cited by 4 publications

References 45 publications

Expression Pattern of Cytokines in Patients with Chronic Hepatitis B Receiving PEGinterferon Therapy

Expression Pattern of Cytokines in Patients with Chronic Hepatitis B Receiving PEGinterferon Therapy

Immunopathology of Chronic Hepatitis B Infection: Role of Innate and Adaptive Immune Response in Disease Progression

CCL17/TARC in autoimmunity and inflammation—not just a T‐cell chemokine

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