ABSTRACT
<p><b>OBJECTIVES</b>To investigate CD3+CD56+ lymphocytes and their subsets in the peripheral blood of chronic hepatitis B patients and to explore the relationship between these cells and the pathogenesis of their diseases.</p><p><b>METHODS</b>Blood samples from 53 chronic hepatitis B patients, 17 from HBV asymptomatic carriers (ASC) and 19 from healthy controls (HC) were collected. CD3+CD56+ lymphocytes were detected by flow cytometry (FCM), then the CD3+CD56+ lymphocytes were gathered to analyze their expressions of CD4, CD8, TCR Valpha24, TCRalpha/beta and TCRgamma/delta.</p><p><b>RESULTS</b>The number of CD3+CD56+ lymphocytes of chronic hepatitis B patients (7.4+/-4.6%) was more than those of ASC (4.5%+/-3.5%) and healthy controls (4.4%+/-3.7%). The expressions of TCR Valpha24 on CD3+CD56+ lymphocytes showed no significant differences among the three groups, but the expression of TCR Valpha24 on CD3-CD56+ lymphocytes of ASC ( 2.8%+/-1.4% ) was much more than that of the HC (1.7%+/-1.0%). For the subsets analysis, the CD8 and TCRalpha/beta subsets of CD3+CD56+ lymphocytes of chronic hepatitis B (61.9%+/-16.8% and 68.1%+/-16.9%) were significantly higher than those of the HC (49.2%+/-15.6% and 56.4%+/-17.9%), while the TCRgamma/delta subsets of chronic hepatitis B and ASC (29.6%+/-15.4% and 30.5%+/-14.8%) were decreased significantly than those of the HC (41.4%+/-19.4%). On the other hand, the CD8 and TCRalpha/beta subsets of CD3+CD56+ lymphocytes of severe chronic hepatitis B (69.0%+/-14.0% and 76.1%+/-12.9%) and CD8 subsets of moderate chronic hepatitis B patients (66.4%+/-14.9%) were significantly higher than those of the mild chronic hepatitis B patients (51.4%+/-16.2% and 62.1%+/-14.6%).</p><p><b>CONCLUSION</b>The pathogenesis of chronic hepatitis B may positively relate to the high expression of CD8 on the CD3+CD56+ lymphocytes.</p>
Subject(s)
Adult , Female , Humans , Male , Middle Aged , Young Adult , CD3 Complex , Allergy and Immunology , CD56 Antigen , Allergy and Immunology , CD8-Positive T-Lymphocytes , Allergy and Immunology , Case-Control Studies , Hepatitis B, Chronic , Allergy and Immunology , Pathology , T-Lymphocyte Subsets , Allergy and Immunology , T-Lymphocytes, Regulatory , Allergy and ImmunologyABSTRACT
<p><b>OBJECTIVE</b>To describe a novel mechanism for TRAIL up-regulation of CD4+, CD8+ T cells to participate in the pathophysiological process in patients with chronic hepatitis B (CHB).</p><p><b>METHODS</b>The serum levels of soluble TRAIL (sTRAIL), IFN-gamma and membrane bound TRAIL expression on peripheral leucocytes from 58 CHB patients were examined by ELISA and flow cytometry respectively. The levels of TRAIL were compared with the baseline levels of 15 healthy controls, and correlation analysis were performed between ALT, TBil and PT, morphological change in hepatic tissues.</p><p><b>RESULTS</b>The results showed that TRAIL levels on membranes of CD4+, CD8+ T cells in CHB patients were much higher than the healthy controls (P < 0.001), which of CD4+ T cells positively correlated with serum TBil (r=0.354, P = 0.008), Serum IFN-gamma level (r=0.302, P = 0.011) and which of CD8+ T cells positively correlated with serum TBil (r=0.522, P = 0.000), ALT (r=0.393, P = 0.003), PT (r=0.385, P = 0.004), serum IFN-gamma level (r=0.307, P = 0.009). The serum levels of soluble TRAIL only correlated with serum HBeAg expression (r=0.695, P = 0.001).</p><p><b>CONCLUSION</b>These findings suggest that the expression of TRAIL on the membranes of lymphocytes was up-regulated, which may take part in the immunopathogenesis in CHB patients. TRAIL expression can be induced either by virus-specific protein expression or by inflammation cytokine IFN-gamma</p>
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Apoptosis Regulatory Proteins , CD4-Positive T-Lymphocytes , Chemistry , CD8-Positive T-Lymphocytes , Chemistry , DNA, Viral , Blood , Hepatitis B, Chronic , Allergy and Immunology , Pathology , Interferon-gamma , Blood , Membrane Glycoproteins , Blood , TNF-Related Apoptosis-Inducing Ligand , Tumor Necrosis Factor-alpha , Up-RegulationABSTRACT
<p><b>OBJECTIVE</b>To realize human immunodeficiency virus(HIV) and hepatitis C virus(HCV) super-infected with hepatitis G virus(HGV or GBV/C) and to probe into the mechanism of these virus infection in the body.</p><p><b>METHODS</b>HIV and HCV load were tested by the quantitated RT-PCR in the HIV or HCV infected plasma samples respectively and the HGV RNA was detected in all of the samples. Then some of the HGV positive were sequenced.</p><p><b>RESULTS</b>123 of 317 HIV patients were positive for HGV, the positive rate was 38.8%. Among the 91 HCV patients, 19 were positive for HGV. The positive rate is 20.9% which was less than that of HIV patients. HIV load of the patients super-infected with HGV was less than that of those without HGV[(1.8+/-0.6)x10 copies/ml compared with (1.9+/-1.1)x10(2)copies/ml]; while HGV and HCV super-infection did not influence the HCV RNA load significantly [(1.5+/-0.6)x10(4) copies/ml compared with (5.4+/-1.8)x10(4)copies/ml]. The HGV sequences from HIV or HCV patients were compared and showed no difference markedly.</p><p><b>CONCLUSION</b>The rate of the HIV and HGV super-infection is higher than that of HCV. HGV may inhibit HIV reproduction in the body while superinfection.</p>