Flow cytometry CD4+/CD8+ ratio of liver-derived lymphocytes correlates with viral replication in chronic hepatitis B

Pham, Bach Nga; Mosnier, Jean‐François; Walker, Francine; Njapoum, C.; Bougy, F.; Degott, Claude; Erlinger, S; Cohen, J; Degos, Françoise

doi:10.1111/j.1365-2249.1994.tb06102.x

Cited by 24 publications

(11 citation statements)

References 25 publications

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“…There was no correlation between the CD4'/CD8^ ratio of liver-derived lymphocytes and the CD4*/CD8+ ratio of peripheral blood lymphocytes. This supports our previous results [27], thereby indicating that lymphocytes we collected from the liver do not reflect blood contamination and assuming Ihat the peripheral blood T cell population may not be represertativc of events occurring in liver tissue.…”

Section: Discussionsupporting

confidence: 89%

“…It has been suggested that T lymphocytes mediate liver cell necrosis [40]. Recently, we have shown that CD4 V<-'D8' ratio of liver-derived lymphocytes but not the percentage of 7/5 TCR T cells or that of CD2^CD57+ correlates with HBV replication in patients with chronic hepatitis B [27]. Therefore, it is tempting to suggest that, in comparison with chronic hepatitis B, liver cell lesions in HCV-infected patients are related to immune-mediated mechanisms.…”

Section: Discussionmentioning

confidence: 84%

“…As the presence of tnononuciear cell infiltrates is a common feature of chronic hepatitis C, intrahepatic T cell subsets were investigated for viraemia and HCV type infection. This study was performed using flow cytometry [27]. The method used for liver-derived lymphocyte analysis in this study avoided a lymphocyte isolation procedure which might lead to cell loss and bias the proportions of lymphoid subpopulation.…”

Section: Discussionmentioning

confidence: 99%

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CD4+/CD8+ ratio of liver-derived lymphocytes is related to viraemia and not to hepatitis C virus genotypes in chronic hepatitis C

Pham

Martinot‐Peignoux

Mosnier

et al. 1995

Clinical and Experimental Immunology

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SUMMARYThe pathogenic mechanisms that lead to chronic hepatitis C are unknown. As hepatitis C virus (HCV) has been shown to induce T cell response, we assessed whether a partictilar T lymphocyte subset could be preferentially detected in theliver of patients with chronic hepatitis C in relation to viraemia or HCV genotypes. The immunophenotypes of liver-derived lymphocytes were analysed in 26 patients by flow cytometry and immunohistochemistry. Viraemia was quantified by branched DNA assay. Using this assay, HCV RNA was not detectable in six patients. HCV RNA was detected in 20 patients, and titres ranged from 8 to 137 x 10''Eq/ml. Genotyping was performed using a line probe assay. Type la. lb. 2a, 3a and 4a were found to infect 2. 10. 2, 7 and 3 patients, respectively. The CD4 ^ /CD8 * ratio of liver-derived lymphocytes was significantly higher [P < 001) in patients with detectable viraemia than in patients without detectable viraemia. In contrast, neither the percentage of ^/i^ T lymphocytes nor that of CD2^CD57^ cells was different in the groups. When comparing the CD4^/CD8^ ratio, the percentage of-y/^ T lymphocytes or CD2^CD57' cells according to genotype, the differences were not significant. These results suggest that the CD4^/ CD8"^ratio of liver-derived lymphocytes is related to viraemia but not to HCV genotypes in patients with chronic hepatitis C. and that T lymphocytes may be involved in the pathogenesis of liver le.sions in chronic hepatitis C, Keywords hepatitis C virus chronic hepatitis C liver-derived lymphocytes lymphocyte subsets viraemia hepatitis C virus genotype

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 84%

Section: Discussionmentioning

confidence: 99%

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CD4+/CD8+ ratio of liver-derived lymphocytes is related to viraemia and not to hepatitis C virus genotypes in chronic hepatitis C

Pham

Martinot‐Peignoux

Mosnier

et al. 1995

Clinical and Experimental Immunology

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“…Boni et al [32][33][34][35] reported that antiviral treatment can overcome CD8 + T cell hypo-responsiveness in subjects with chronic HBV infection, suggesting that the T cells are present, but suppressed. It was reported by Pham et al [36] in 21 CHB patients that the ratio of CD4 + / CD8 + liver-derived lymphocytes, and not of peripheral blood lymphocytes appeared to be related to the level of HBV replication, and it revealed a positive correlation with viral load. The evidence that efficient antiviral T cell response can be restored by mono-antiviral treatment in CHB patients concurrently with reduction of viremia, indicates the importance of viral load in the pathogenesis of T cell hypo-responsiveness in these patients.…”

Section: Discussionmentioning

confidence: 84%

Hepatitis B virus DNA is more powerful than HBeAg in predicting peripheral T-lymphocyte subpopulations in chronic HBV-infected individuals with normal liver function tests

You¹,

Sriplung²,

Geater³

et al. 2008

WJG

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AIM:To investigate the peripheral T-lymphocyte subpopulation profile, and its correlations with hepatitis B virus (HBV) replication level in chronic HBV-infected (CHI) individuals with normal liver function tests (LFTs). METHODS: Frequencies of T-lymphocyte subpopulations in peripheral blood were measured by flow cytometry in 216 CHI individuals. HBV markers were detected with ELISA. Serum HBV DNA load was assessed with quantitative real-time PCR. Information of age at HBV infection, and maternal HBV infection status was collected. ANOVA linear trend test and linear regression were used in statistical analysis. RESULTS: CHI individuals had significantly decreased relative frequencies of CD3 + , CD4 + subpopulations and CD4 + /CD8 + ratio, and increased CD8 + subset percentage compared with uninfected individuals (all P < 0.001). There was a significant linear relationship between the load of HBV DNA and the parameters of T-lymphocyte subpopulations (ANOVA linear trend test P < 0.01). The parameters were also significantly worse among individuals whose mothers were known to be HBV carriers, and those having gained infection before the age of 8 years. In multiple regressions, after adjustment for age at HBV infection and status of maternal HBV infection, log copies of HBV DNA maintained its highly significant predictive coefficient on T-lymphocyte subpopulations, whereas the effect of HBeAg was not significant. CONCLUSION: HBV DNA correlates with modification in the relative T-lymphocyte subpopulation frequencies. High viral load is more powerful than HBeAg in predicting the impaired balance of T-cell subsets.

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“…Boni et al [38,39] have reported antiviral treatment can overcome CD8 + T-cell hyporesponsiveness in subjects with CHB, which suggests the T cells are present but suppressed. It has been reported by Pham et al [40] in 21 CHB patients that the ratio of CD4 + /CD8 + liver-derived lymphocytes, but not of peripheral blood lymphocytes, appears to be related to the level of HBV replication, which reveals a positive correlation with viral load. The evidence that an efficient antiviral T-cell response can be restored by antiviral monotherapy in CHB, concurrently with reduction of viremia, indicates the importance of viral load in the pathogenesis of T-cell hyporesponsiveness.…”

Section: Figurementioning

confidence: 81%

Effect of viral load on T-lymphocyte failure in patients with chronic hepatitis B

You¹,

Sriplung²,

Geater³

et al. 2008

WJG

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AIM:To investigate peripheral T-lymphocyte subpopulation profile and its correlation with hepatitis B virus (HBV) replication in patients with chronic hepatitis B (CHB). METHODS:Distribution of T-lymphocyte subpopulations in peripheral blood was measured by flow cytometry in 206 CHB patients. HBV markers were detected with ELISA. Serum HBV DNA load was assessed with quantitative real-time polymerase chain reaction (PCR). The relationship between HBV replication and variation in peripheral T-cell subsets was analyzed. showed a similar pattern of these parameters was significantly associated with high viral load, presence of serum hepatitis B e antigen (HBeAg) expression, liver disease severity, history of maternal HBV infection, and young age at HBV infection, all with P < 0.01. There was a significant linear relationship between viral load and these parameters of T-lymphocyte subpopulations (linear trend test P < 0.001). There was a negative correlation b e t w e e n t h e l e ve l s o f C D 3 + a n d C D 4 + c e l l s a n d CD4 + /CD8 + ratio and serum level of viral load in CHB patients (r = -0.68, -0.65 and -0.75, all P < 0.0001), and a positive correlation between CD8 + cells and viral load (r = 0.70, P < 0.0001). There was a significant decreasing trend in CD3 + and CD4 + cells and CD4 + /CD8 + ratio with increasing severity of hepatocyte damage and decreasing age at HBV infection (linear trend test P < 0.01). In multiple regression (after adjustment for age at HBV infection, maternal HBV infection status and hepatocyte damage severity) log copies of HBV DNA maintained a highly significant predictive coefficient on T-lymphocyte subpopulations, and was the strongest predictor of variation in CD3 + , CD4 + , CD8 + cells and CD4 + /CD8 + ratio. However, the effect of HBeAg was not significant. RESULTS CONCLUSION:T-lymphocyte failure was significantly associated with viral replication level. The substantial linear dose-response relationship and strong independent predictive effect of viral load on T-lymphocyte subpopulations suggests the possibility of a causal relationship between them, and indicates the importance of viral load in the pathogenesis of T cell hyporesponsiveness in these patients.

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Flow cytometry CD4+/CD8+ ratio of liver-derived lymphocytes correlates with viral replication in chronic hepatitis B

Cited by 24 publications

References 25 publications

CD4+/CD8+ ratio of liver-derived lymphocytes is related to viraemia and not to hepatitis C virus genotypes in chronic hepatitis C

CD4+/CD8+ ratio of liver-derived lymphocytes is related to viraemia and not to hepatitis C virus genotypes in chronic hepatitis C

Hepatitis B virus DNA is more powerful than HBeAg in predicting peripheral T-lymphocyte subpopulations in chronic HBV-infected individuals with normal liver function tests

Effect of viral load on T-lymphocyte failure in patients with chronic hepatitis B

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