scholarly journals Programmed Cell Death Protein 1-overexpressed CD8+ T Lymphocytes Play a Role in Increasing Chronic Hepatitis B Disease Progression

2021 ◽  
Vol 13 (3) ◽  
pp. 310-5
Author(s):  
Fatmawati Fatmawati ◽  
Ellyza Nasrul ◽  
Nasrul Zubir ◽  
Ferry Sandra

BACKGROUND: T lymphocyte activation depends on the balance of co-stimulatory and co-inhibitory signals determined by Cluster of Diffrentiation (CD)28 and Programmed Cell Death Protein 1 (PD-1) expression. Alteration in CD28 and PD-1 expression might affect the progression of chronic hepatitis B (CHB). Current study was conducted to evaluate the correlations of the CD28 and PD-1 expressions of T lymphocytes and CHB progression.METHODS: Subjects were recruited, selected and divided into 3 groups, inactive CHB, active CHB and CHB with End-Stage Liver Disease (ESLD). HBeAg was determined by using Enzyme-Linked Fluorescence Assay while HBV-DNA was carried out by the RT-PCR method. Numbers of T lymphocytes expressing CD3, CD4, CD8, CD45, CD28 and PD-1 molecules were determined by flowcytometry. RESULTS: There was no significant difference in the expression of CD28 by CD4+ and CD8+ T lymphocytes of inactive CHB, active CHB and CHB with ESLD subjects. There was also no significant difference in the expression of PD-1 in CD4+ lymphocytes of inactive CHB, active CHB and ESLD subjects. In contrast there was a significant increase in the expression of PD-1 in CD8+ T lymphocytes of ESLD subjects.CONCLUSION: CD28 expression among CHB subjects was within normal range and not related to disease progression, but PD-1 expression of CD8+ T lymphocyte was increased along with disease progression, especially in CHB subjects with ESLD. This suggests that PD-1-overexpressed CD8+ T lymphocyte play a role in increasing CHB disease progression.KEYWORDS: chronic hepatitis B, CD28, PD-1, T lymphocyte, disease progression

2003 ◽  
Vol 72 (2) ◽  
pp. 215-222 ◽  
Author(s):  
Thjon J. Tang ◽  
Robert A. de Man ◽  
Johannes G. Kusters ◽  
Jaap Kwekkeboom ◽  
Wim C.J. Hop ◽  
...  

2005 ◽  
Vol 43 (1) ◽  
pp. 45-52 ◽  
Author(s):  
Thjon J. Tang ◽  
Jaap Kwekkeboom ◽  
Shanta Mancham ◽  
Rekha S. Binda ◽  
Robert A. de Man ◽  
...  

Author(s):  
Hairul Anwar ◽  
Mutmainnah Mutmainnah ◽  
Ibrahim Abdul Samad

Chronic hepatitis B is an infectious liver disease caused by hepatitis B virus that persist for more than 6 months. Fibrosis is a result of fibrogenesis which is the formation of connective tissue (scarring) caused by liver tissue damage. Liver damage will affect the production of thrombopoetin causing disturbances in the balance between destruction and production of platelet resulting in decreased platelet counts. This study was a retrospective cross-sectional study by taking the data from medical records of chronic hepatitis B patients who were tested for complete blood count and fibroScan at the Dr.Wahidin Sudirohusodo Hospital Makassar from January 2014 to July 2016. The result showed a total of 323 chronic B hepatitis patients, 99 with severe fibrosis, 84 with moderate fibrosis and 140 with mild fibrosis. The Spearman correlation test showed a significant correlation between the platelet count and the degree of fibrosis (p <0.001) and showed a positive correlation between both of them with a very strong correlation (r = 0.802). The Kruskal-Wallis test showed a significant difference between platelet count and the degree of fibrosis (p<0.001). The conclusion is that a decreased platelet count is a sign of an increase in the degree of fibrosis in chronic hepatitis B patients. It is suggested to perform another study with larger samples based on the degree of fibrosis. 


2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Hui-Lian Wang ◽  
Xi Lu ◽  
Xudong Yang ◽  
Nan Xu

The relative efficacy of different strategies for chronic hepatitis B (CHB) patients with lamivudine resistance (LAM-R) has not yet been systematically studied. Clinical trials were searched in PUBMED, MEDLINE, EMBASE, and CNKI databases up to February 15, 2016. Nine trials including 764 patients met the entry criteria. In direct meta-analysis, TDF showed a stronger antiviral effect than any one of ETV, LAM/ADV, and ADV against LAM-R hepatitis B virus. LAM/ADV therapy was superior to ADV in suppressing viral replication. ETV achieved similar rate of HBV DNA undetectable compared to ADV or LAM/ADV. In network meta-analysis, TDF had higher rates of HBV DNA undetectable compared to ETV (OR, 24.69; 95% CrI: 5.36–113.66), ADV (OR, 37.28; 95% CrI: 9.73–142.92), or LAM/ADV (OR, 21.05; 95% CrI: 5.70–77.80). However, among ETV, ADV, and LAM/ADV, no drug was clearly superior to others in HBV DNA undetectable rate. Moreover, no significant difference in the rate of ALT normalization or HBeAg loss was observed compared the four rescue strategies with each other. TDF appears to be a more effective rescue therapy than LAM/ADV, ETV, or ADV. LAM plus ADV therapy was a better treatment option than ETV or ADV alone for patients with LAM-R.


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