Detection of T lymphocyte subsets and mIL-2R on surface of PBMC in patients with hepatitis B

Wang, Ke-xia; Peng, Jiang-Long; Wang, Xuefeng; Tian, Ye; Wang, Jian; Chao-pin, LI

doi:10.3748/wjg.v9.i9.2017

Cited by 15 publications

(13 citation statements)

References 44 publications

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“…Our findings indicate that normal LFTs chronic HBV-infected individuals have an impaired balance of T-cell profile. The same finding also has been proved by previous researches in patients with chronic hepatitis B (CHB) that the chronicity of HBV infection is caused by a deficiency in cellular immune function, and hepatocytic damage is mainly caused by immunological injury [12][13][14][15][16][17][18][19][20][21] . However, the mechanism has not been defined [5] .…”

Section: Discussionsupporting

confidence: 61%

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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Section: Discussionsupporting

confidence: 61%

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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show abstract

“…Our findings indicate that CHB patients have T-cell failure. The same finding has also been demonstrated previously, namely, that the chronicity of HBV infection is caused by a deficiency in cellular immune function [16][17][18][19][20] , and hepatocyte damage is mainly caused by immunological injur y [21][22][23][24][25][26][27][28][29] . However, the mechanism has not been defined [5] .…”

Section: Figuresupporting

confidence: 65%

“…Therefore, immune elimination of infected cells can lead to the termination of infection when it is efficient, or to a persistent necroinflammatory disease when it is not [47] . Destruction of infected cells, however, is not the only mechanism implicated in the elimination of intracellular virus, as demonstrated by studies carried out in animal models of HBV infection and in human hepatitis B, which demonstrate the importance of cytokine-mediated, noncytolytic mechanisms of anti-viral protection [20][21][22][23][24][25][26][27][28][29][30][31] .…”

Section: Figurementioning

confidence: 99%

“…Hepatocyte damage may also be correlated directly with T-cell failure, rather than through the load copies of viral replication. Previous studies have suggested that hepatocyte damage is mainly caused by immunological injury [9,[21][22][23][24][25][26][27][28][29][30] . HBV is a typical non-cytopathic virus that can induce tissue damage of variable severity by stimulating a protective immune response that can simultaneously cause damage and protection, by killing an intracellular virus through the destruction of virus-infected cells [5] .…”

Section: Figurementioning

confidence: 99%

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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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“…The host’s response through cell-mediated immunity rather than a direct cytopathic effect of the virus is said to be responsible for the damage to infected hepatocytes 1. Peripheral blood mononuclear cells containing an aggregate of immune-competent cells, including subsets of T lymphocytes, natural killer cells, and lymphokine-activated killer T cells, are thought to play an important role in the persistence or control of HBV infection 2,3. Moreover, a strong association between cytotoxic T cells, liver cell damage, and HBV clearance has also been demonstrated 4,5.…”

Section: Introductionmentioning

confidence: 99%

Relationship between serum HBsAg level, HBV DNA level, and peripheral immune cells in patients with chronic hepatitis B virus infection

Mukherjee¹,

Reddy²,

Arava³

et al. 2010

HMER

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BackgroundThe chronicity of hepatitis B virus (HBV) infection is attributed to inappropriate functioning of cell-mediated immunity. Besides the importance of measuring serum HBV DNA and HBV surface antigen (HBsAg) as markers of viral replication and exposure, respectively, studies regarding their influence on immune cell status in chronic HBV infection are still scarce. Because such studies of chronic HBV patients have not been reported for India, we attempted to evaluate the relationship between serum concentrations of HBsAg, HBV DNA, and percentage of immune cells in peripheral blood of Indian subjects with chronic HBV infection.MethodsThirty-one HbsAg-positive subjects were evaluated for serum HBe antigen (HBeAg), anti-HBe, and alanine transferase status by standard enzyme-linked immunosorbent assay (ELISA) and biochemical procedures. Serum HBV DNA level was determined by real-time TaqMan® polymerase chain reaction assay. Serum HBsAg level was measured by a third-generation sandwich ELISA kit. Peripheral immune cell profiling was done by multifluorometric flow cytometry analysis, for which 21 healthy subjects were included as controls.ResultsThe majority (93.5%) of the study subjects were HBeAg-negative and anti-HBeAg-positive. Mean viral load, HBsAg, and alanine transferase levels were 4.20 ± 1.96 log copies/mL, 5.98 ± 4.62 log IU/mL, and 74.5 ± 110 IU/mL, respectively. In comparison with controls, total T cell and cytotoxic T cell populations were significantly (P < 0.05) reduced in HBV-infected subjects, while the status of B cells, natural killer cells, T helper cells, and ratio of T helper to cytotoxic cells remained unaltered.ConclusionSuppression of the peripheral cytotoxic T cell population in chronic HBeAg-negative chronic HBV infection is influenced by increased viral load. Serum HBsAg concentration appeared independent of serum HBV DNA level and immune cell status. Nonelevation of natural killer cell and T helper cell numbers in subjects harboring lower to moderate HBV loads is further indicative of noninduction of innate as well as a coordinated adaptive immune response favoring chronicity of the disease.

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Detection of T lymphocyte subsets and mIL-2R on surface of PBMC in patients with hepatitis B

Abstract: Both cellular and humoral immune functions are obviously in disorder in patients with hepatitis B, which might be closely associated with the chronicity in patients.

Cited by 15 publications

References 44 publications

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

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

Relationship between serum HBsAg level, HBV DNA level, and peripheral immune cells in patients with chronic hepatitis B virus infection

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