Chronic hepatitis B (CHB) infection remains a significant global public health concern. Functional cure, defined as hepatitis B surface antigen seroclearance with unquantifiable HBV DNA at 24 weeks off treatment, is a desirable endpoint in the treatment of CHB, yet challenging to achieve. Given the limitations of current therapies including nucleos(t)ide analogues and pegylated interferon alpha, novel agents targeting functional cure are emerging. As hepatitis B virus (HBV) is a non-cytolytic virus, liver damage stems from the host immune response towards HBV-infected cells. The innate immune response during the initial phase of HBV infection is crucial in establishing an adequate level of immunity against the virus. However, HBV adopts various mechanisms to evade the host’s innate immunity, partly contributing to the chronicity of infection. This article provides a comprehensive review on how the HBV life cycle interacts with the host’s innate immune system. The latest evidence of novel agents targeting the innate immunity will also be covered. Retinoic acid inducible gene I agonists, toll-like receptor agonists, and interferons are therapies that target the HBV evasion strategies against host’s innate immunity. While small interfering RNAs and antisense oligonucleotides are originally designed for antigen knockdown and reinvigoration of the adaptive immune response, they have also shown additional impacts on the innate immunity. With ongoing research and innovation in combination strategies, advancement in the management of CHB is anticipated in the future.
Steatotic liver diseases (SLD) are the principal worldwide cause of cirrhosis and end-stage liver cancer, affecting nearly a quarter of the global population. SLD includes metabolic dysfunction-associated alcoholic liver disease (MetALD) and metabolic dysfunction-associated steatotic liver disease (MASLD), resulting in asymptomatic liver steatosis, fibrosis, cirrhosis and associated complications. The immune processes include gut dysbiosis, adiposeliver organ crosstalk, hepatocyte death and immune cell-mediated inflammatory processes. Notably, various immune cells such as B cells, plasma cells, dendritic cells, conventional CD4+ and CD8+ T cells, innate-like T cells, platelets, neutrophils and macrophages play vital roles in the development of MetALD and MASLD. Immunological modulations targeting hepatocyte death, inflammatory reactions and gut microbiome include N-acetylcysteine, selonsertib, F-652, prednisone, pentoxifylline, anakinra, JKB-121, HA35, obeticholic acid, probiotics, prebiotics, antibiotics and fecal microbiota transplantation. Understanding the immunological mechanisms underlying SLD is crucial for advancing clinical therapeutic strategies.
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Two major causes of steatohepatitis are alcohol and metabolic syndrome. Although the underlying causes of alcoholrelated liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD)/nonalcoholic steatohepatitis (NASH) differ, there are certain similarities in terms of the mode of disease progression and underlying pathophysiological mechanisms. Further, excessive alcohol consumption is often seen in patients with metabolic syndrome, and alcoholic hepatitis exacerbation by comorbidity with metabolic syndrome is an emerging clinical problem. There are certain ethnic differences in the development of both NAFLD and ALD. Especially, Asian populations tend to be more susceptible to NAFLD, and genetic polymorphisms in patatin-like phospholipase domain-containing 3 (PNPLA3) play a key role in both NAFLD and ALD. From the viewpoint of pathophysiology, cellular stress responses, including autophagy and endoplasmic reticulum (ER) stress, are involved in the development of cellular injury in steatohepatitis. Further, gutderived bacterial products and innate immune responses in the liver most likely play a profound role in the pathogenesis of both ALD and NASH. Though the recent progress in the treatment of viral hepatitis has reduced the prevalence of viral-related development of hepatocellular carcinoma (HCC), non-viral HCC is increasing. Alcohol and metabolic syndrome synergistically exacerbate progression of steatohepatitis, resulting in carcinogenesis. The gut-liver axis is a potential therapeutic and prophylactic target for steatohepatitis and subsequent carcinogenesis.
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Oromucosal cytokine therapy allows large amounts of cytokines to be administered with improved outcome and without dose limiting toxicity. Orally administered cytokines exert their effects by a novel two pronged mechanism of action. Firstly, specific populations of immuno-competent effector cells are activated in the oral cavity and migrate to the site of virus replication. Secondly, chemokines produced in the lymphoid tissue of the oral cavity enter the peripheral circulation and redirect activated lymphocytes to eliminate virus infected cells. Oromucosal IFN therapy constitutes an alternative and improved means of therapy for diseases such as chronic viral hepatitis which are currently treated parenterally with IFNα. The oral route also has obvious advantages for ease of administration and improved patient compliance. Furthermore, the availability of a well tolerated form of IFN therapy will also allow Type I IFNs to be used for the treatment of diseases such as upper respiratory tract virus infections, for which parenteral IFN therapy is currently precluded due to unacceptable toxicity.(Korean J Hepatol 2002;8:125-131)
Hepatitis C virus (HCV) infection is a worldwide problem in terms of public health. It causes chronic hepatitis C in 60-80% of patients after acute hepatitis C. Chronic hepatitis C can progress to liver cirrhosis and hepatocellular carcinoma. In the present time, combination therapy of pegylated interferon-α and ribavirin is the standard therapy for hepatitis C, but it results in sustained virologic response only in 45-80% of treated patients. In addition, there is no available effective vaccine for HCV. To develop effective immunotherapy or preventive vaccine, understanding of the immune response against HCV is prerequisite. Among several components of immune system, T cells play a key role in the clearance of HCV and immunopathology during hepatitis C. In the study of HCV infection, however, the most important limiting factor is the absence of small animal model as only humans and chimpanzees can be infected by HCV. In this review, T cell response against HCV, which has been known from the studies of the HCV-infected patients and chimpanzees, will be discussed in several circumstances, including acute hepatitis C, chronic hepatitis C and recovered status from hepatitis C. (Korean J Hepatol 2006;12:140-153)
Hepatitis B virus (HBV) currently infects more than 400 million people worldwide and they are at risk of developing chronic liver disease, cirrhosis and hepatocellular carcinoma. The immune response to HBV- encoded antigens is responsible both for viral clearance and for disease pathogenesis during HBV infection. While the humoral antibody response to viral envelope antigens contributes to the clearance of circulating virus particles, the cellular immune responses to the envelope, nucleocapsid, and polymerase antigens were known to eliminate virus in infected hepatocytes through cytolytic as well as noncytolytic mechanisms. Liver injury could be initiated by an immune response against HBV, but mainly resulted from HBV non-specific lymphocytes and macrophages. There are growing evidences that T helper 1 memory T cells play a predominant role in suppressing viral replication mainly by IFN-γ through noncytolytic antiviral mechanism. Elucidation of the immunological and virological basis for HBV infection may yield effective immunotherapeutic and antiviral strategies to terminate chronic HBV infection. (Korean J Hepatol 2006;12: 154-162)
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