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Journal : The Indonesian Journal of Gastroenterology, Hepatology and Digestive Endoscopy

A Systematic Review of the Frequency of Regulatory T Cells in Hepatitis B and Hepatitis C Tri Nugraha Susilawati; Atik Susianto
The Indonesian Journal of Gastroenterology, Hepatology, and Digestive Endoscopy Vol 20, No 3 (2019): VOLUME 20, NUMBER 3, December 2019
Publisher : The Indonesian Society for Digestive Endoscopy

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (173.471 KB) | DOI: 10.24871/2032019161-168

Abstract

Background: Regulatory T cells (Tregs) play an important role in sustaining the hepatitis B and C viruses (HBV and HCV) persistence and protecting the liver tissues from cytokine-associated detrimental effects through unclear mechanisms. This paper aims to review the frequency of Tregs during the course of HBV and HCV infection.Method: Electronic databases were searched to identify studies investigated the frequency of intrahepatic and peripheral Tregs of the patients infected with HBV and/ or HCV.Results: The majority of studies reported the increase of intrahepatic and peripheral Tregs in acute and chronic infection of HBV and HCV. The decrease of peripheral Tregs occurred in patients with chronic hepatitis B who respond to interferon α or nucleos(t)ide analogues treatment as well as those with chronic hepatitis C who were treated with interferon, ribavirin or liver transplantation.Conclusion: Infection with HBV and HCV appears to induce the production of Tregs in blood and hepatocytes whereas treatment may decrease Tregs levels. As the optimum balance between regulatory and effector T during HBV and HCV infection is crucial for preventing liver damage, further studies should be directed on the development of Tregs during HBV and HCV infection as well as their involvement in immunomodulatory strategies for combating HBV and HCV.
The Prevalence of T Cells Population in the Liver of Patients with Viral Hepatitis Tri Nugraha Susilawati; Triyanta Yuli Pramana; Brian wasita
The Indonesian Journal of Gastroenterology, Hepatology, and Digestive Endoscopy Vol 21, No 1 (2020): VOLUME 21, NUMBER 1, April 2020
Publisher : The Indonesian Society for Digestive Endoscopy

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (153.418 KB) | DOI: 10.24871/211202033-37

Abstract

Background: It has been widely known that viral hepatitis is a major cause of liver disease that can cause chronic inflammation and carcinoma. This study aimed to describe the frequencies of CD4+ and CD8+ T cells, as well as regulatory T cells (CD25+ and Foxp3+ T cells) in the liver of patients with viral hepatitis in order to understand the comprehensive role of T lymphocytes in the progression of liver diseases attributed to viral hepatitis.Method: Liver biopsies were performed on adult patients presenting to a tertiary hospital in Surakarta, Indonesia with viral hepatitis from 2017 to 2018. Immunohistochemical staining was performed to identify cells expressing CD4+, CD8+, CD25+and Foxp3+ which represent T helper, T cytotoxic, and T regulatory cells, respectively. Additional data were retrieved from the patients’ medical records, including alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, viral load, and results of ultrasonography and fibroscan.Results: A total of 25 liver samples were collected from patients with chronic HBV infection (n = 21), chronic HCV infection (n = 2), acute HBV infection (n = 1), and from a with multiple liver nodules. The liver injury is minimum in all patients. The study found that CD8+ and CD4+ T cells were predominant whilst the frequency of T regulatory cells is generally low.Conclusions: The findings indicate the involvement of intrahepatic T helper and T cytotoxic in the pathogenesis of viral hepatitis. These liver infiltrating T cell subsets may be readily differentiated into regulatory T cells expressing CD25+ and Foxp3+ in order to prevent severe inflammation and maintain disease chronicity.
Proinflammatory Cytokines and Its Correlation with Liver Injury Tri Nugraha Susilawati; Winda Rahayuningtyas; Triyanta Yuli Pramana
The Indonesian Journal of Gastroenterology, Hepatology, and Digestive Endoscopy Vol 22, No 3 (2021): VOLUME 22, NUMBER 3, December 2021
Publisher : The Indonesian Society for Digestive Endoscopy

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (6094.133 KB) | DOI: 10.24871/2232021210-216

Abstract

Background: A persistent infection of hepatitis B virus (HBV) can cause liver cirrhosis and hepatocarcinoma even though the virus itself is non-cytopathic and does not cause cell injury. It has been asserted that liver injury in chronic HBV infection is attributed to the host immune system responding to HBV infection. Cytokines have a critical role in mediating immune responses to viral infection. This study aimed to determine the correlation between the levels of serum IFN-γ, IL-2, IL-17, and TNF- α with the progress of chronic HBV infection that was determined through provisional diagnosis, patient’s age, and the levels of serum transaminases.Method: Blood samples were collected from patients with chronic hepatitis B and the levels of serum IFN-γ, IL-2, IL-17, and TNF-α were measured by using ELISA. The correlation between each cytokine levels and the provisional diagnosis, patient’s age, and serum transaminases were analyzed by using the Spearman correlation test with a p value of 0.05 is considered as statistically significant.Results: A total of 47 samples were collected from patients with chronic hepatitis B (n=38), chronic hepatitis B with liver cirrhosis (n = 6), and chronic hepatitis B with hepatocellular carcinoma (nc = 3). A significant correlation was found between the levels of serum IFN-γ and aspartate aminotransferase (AST) (p = 0.04).Conclusion: The increase of serum IFN-γ and AST levels may highlight the importance of these particular cytokine and liver transaminase in the immune response to chronic HBV infection since IFN-γ is capable to induce apoptotic cell death which promotes AST release and facilitates liver injury.