Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Long-term cultured T-cells, reactive to Pre-S1 protein, were developed from peripheral blood mononuclear cells (PBMC) of individuals after recovery from hepatitis B infection and of vaccine recipients by in vitro Pre-S1 protein stimulation in the presence of IL-2. The proliferative responses to Pre-S1 protein and functional activities of cultured T-cells were characterized.
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PMID:Effect of Pre-S1 protein on the long-term cultures of human lymphocytes after hepatitis B immunization. 134 Jan 82

Hepatitis B virus (HBV)-associated nucleocapsid antigen (HB core and HB e) is believed to be a major target for T cell-mediated hepatocellular damage in chronic HBV carriers. Studies were undertaken to determine whether both nucleocapsid Ag could be recognized by T cell lines from peripheral blood mononuclear cells (PBMC) from patients with chronic hepatitis B. After cultivation in the presence of rHBcAg or purified HBeAg, growing cells were cloned by limiting dilution in the presence of PHA, IL-2 and allogenic feeder cells. Four HBcAg-reactive and three HBeAg-reactive T cell lines from two patients were generated by proliferation assays. None of the cell lines responded to HB surface Ag or PPD. Four lines were of the CD8+ CD11b- cytotoxic phenotype, two of the CD4+ Leu8- helper phenotype, and the remaining one consisted of mixed populations of CD4+ Leu8+ and CD4+ Leu8- cells. Cross-reactivity study showed that a HBcAg-induced CD4+ T cell line responded to HBeAg, and similarly a HBeAg-induced CD8+ T cell line responded to HBcAg. The reactions were inhibited by HLA class II antibody, but not by class I Ab.
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PMID:T cell lines reactive with hepatitis B core and E antigens in patients with chronic hepatitis B. 166 81

In an attempt to gain some insight into the many factors influencing antibody gene expression in human B cell lines, we have examined in detail the relationship between cell surface phenotype, cytokines, and the growth and antibody-producing capacity of a panel of immortalized human B cell lines. The cell panel comprised lines secreting either high or low titers of antibodies against Rhesus D, hepatitis B surface, and tetanus toxoid antigens. All the transformed cell lines exhibited a cell surface phenotype characteristic of well-differentiated peripheral blood cells strongly expressing CD23 and CD38 while weakly expressing CD10 and CD21. There was no obvious relationship between the antibody-body-secreting and proliferative capacity of the cell lines and their cell surface phenotype. Antibody secretion by the cells was rarely improved by the addition of a wide range of doses of recombinant IL-2, IL-4, or IL-6. In addition, such treatment frequently inhibited proliferation. Supernatants from some of the cell lines promoted the growth of unrelated cell lines but failed to influence antibody production. Such supernatants contained the highest concentration of IL-1, TNF beta, TGF beta, and soluble CD23. In contrast, the heterohybrid supernatant which inhibited cell growth secreted low levels of these cytokines. None of the cell lines secreted detectable amounts of IL-2, IL-4, INF gamma, or GCSF. There was no obvious relationship between cytokine production and antibody secretion. Finally, LPS had a slight but variable effect on antibody secretion but failed to influence cell growth.
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PMID:Cell surface phenotype, cytokines, and antibody gene expression in immortalized human B cell lines. 210 58

We studied the immunoregulatory mechanisms of responsiveness and non-responsiveness to hepatitis B (HB) vaccine by analysing the influence of HB surface antigen (HBsAg) on lymphokine- or mitogen-stimulated peripheral lymphocytes from healthy volunteers. Stimulation with pokeweed mitogen (PWM) led to a reduced production of polyclonal IgG from responder cells compared to non-responder lymphocytes. PWM did not enhance the HBs-specific IgG production from responder lymphocytes when the cells were obtained at Day 10 after the last vaccination. A slight reduction of the proliferative response was observed when lymphocytes of non-responders were stimulated with phytohaemagglutinin (PHA) or concanavalin A (Con A). Production of HBs-specific antibodies was enhanced by incubating responder lymphocytes with interleukin-4 (IL-4). The HBs antigen itself did not modulate the expression of the CD23 B-cell differentiation antigen in unseparated lymphocytes. However, CD23 expression induced by low doses of IL-4 was markedly enhanced in an antigen-specific way. Our data indicate that HBs antigen enhances the lymphokine-induced CD23 expression, whereas the mitogen-induced CD23 expression is not affected. Lymphocytes obtained from non-responders exerted a reduced expression of CD25 surface antigen compared to responder lymphocytes. Exogeneous addition of IL-2 in the absence or presence of HBsAg induced a marked enhancement of the IL-2 receptor expression in responder lymphocytes. Furthermore, no significant modulation of CD25 expression was observed in non-responder lymphocytes.
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PMID:Effects of mitogens and lymphokines on the regulation of the immune response to HBs antigen in vitro. 214 40

Studies were undertaken to evaluate the effect of hepatitis B virus (HBV) immune complexes (HBV-IC) on IL-2 dependent human lymphocyte proliferation. The following parameters were studied: 1) Effect of HBV-IC (HBsAg-IgG or HBeAg-IgG) on PHA-mediated lymphocyte proliferation; 2) Influence of HBV-IC on the ability of PHA-stimulated peripheral blood lymphocytes (PBL) for IL-2 production and IL-2 receptor expression. HBV-IC induced a dose dependent and antigenic dependent suppression of PHA stimulated lymphocytes. The suppressor effect exerted by HBsAg-IgG was irreversible. In contrast, the suppression mediated by HBeAg-IgG was reversible: lymphocytes preincubated with this preparation washed and activated with PHA responded well to mitogen. The presence of HBV-IC in the cultures of PHA-activated PBL decreased their ability to produce IL-2: HBeAg-IgG exerted a stronger suppressor effect. This effect was partially reversible: removal of HBV-IC from the culture by washing and subsequent stimulation of PBL with PHA increased the capacity of lymphocytes to produce IL-2. This was particularly evident with HBeAg-IgG. Decreased activity of IL-2 observed in the cultures, was also partially dependent on the ability of HBV-IC to bind IL-2 present in the culture medium. Experiments performed using ultracentrifugation indicated that HBV-IC, especially HBsAg-IgG, may bind to IL-2 and inactivate it. HBV-IC had also an effect on IL-2 receptor expression: 1) their presence in the cultures of PHA-stimulated PBL decreased the number of Tac positive cells; 2) the response of HTCL to exogenous IL-2 was decreased by HBV-IC present in the culture medium. This was especially observed in the case of HBsAg-IgG. We suggest that the observed inhibition of PHA-induced lymphocyte proliferation exerted by immune complexes containing HBsAg-IgG or HBeAg-IgG may be caused mainly by their influence on IL-2 dependent mechanism of lymphoproliferation.
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PMID:Influence of immune complexes containing HBsAg and HBeAg on IL-2 dependent human lymphocyte proliferation. 234 99

Anti-hepatitis B surface (HBs) antibodies have been induced in vitro by human peripheral blood mononuclear cells (PBMC) from individuals immunized with hepatitis B surface antigen (HBsAg). Anti-HBs antibody production is antigen-specific, T-cell dependent, class II MHC-restricted and requires de novo synthesis. Furthermore, HBsAg-specific CD8 suppressor cells can also be induced in vitro after challenge with high antigen doses. Antigen presenting cells (APC) are required for the induction of suppression. These suppressor cells are antigen-specific since they do not suppress the antibody response to tetanus toxoid. Antigen-specific suppression is inhibited by cytotoxic treatment of CD8 CD11 cells with OKM1 monoclonal antibody (MoAb) and complement, suggesting that these suppressor CD8 cells may represent granular lymphocytes. Addition to cultures of high concentrations of a recombinant human IL-2 dose not affect suppression, ruling out the adsorption of IL-2 by suppressor cells as a possible mechanism for suppression.
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PMID:In vitro induction of HBsAg-specific CD8 CD11 human suppressor T cells. 244 29

Hepatitis B core (HBc)Ag-specific T cells present in the peripheral blood of a patient with chronic active hepatitis B were expanded by co-cultivation for 7 days with rHBcAg. After cloning at 1 cell/well in the presence of PHA and IL-2, five HBcAg-specific CD4+ cloned lines were obtained. All five lines proliferated and produced IL-2, IFN-gamma, and TNF in a dose-dependent fashion in response to HBcAg, but not to HBV envelope Ag. The cloned lines and derivative clones were HLA class II (DR1) restricted. All T cell clones were able to induce anti-HBc production by autologous B cells in response to HBcAg (helper effect). The proliferative response and the helper effect of the HBcAg-specific T cell lines and clones were augmented by co-cultivation with an autologous, autoreactive (HLA-DQ1 specific) T cell clone, even in the absence of HBcAg, and the autoreactive T cells directly stimulated anti-HBc secretion by autologous B cells, presumably due to the release of Ag-nonspecific factors. These findings define a model immunoregulatory circuit the physiologic significance of which remains to be determined.
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PMID:Functional modulation of hepatitis B core antigen-specific T lymphocytes by an autoreactive T cell clone. 245 43

Clones of HBsAg-reactive CD8+ and CD4+ T cells were obtained from PBM of a hepatitis B immunized individual whose PBM proliferated when cultured with HBsAg. Lymphocytes were activated by culturing for 2 weeks with HBsAg and high concentrations of IL-2, then cloned in the presence of irradiated HBsAg-activated PBM and autologous EBV-transformed B cells, together with antigen and IL-2. All clones examined exhibited proliferation in an antigen-specific manner. Of 7 clones examined by flow cytometry, 4 were CD4+, CD8-; and 3 were CD4-, CD8+. Several clones produced IL-2 activity after stimulation with HBsAg. Since development of CD8+ T-cell clones specific for soluble antigens has been difficult, the high frequency with which CD8+ cells were cloned in these experiments suggests that the cloning strategy employed may have general use for development of CD8+ clones, Availability of HBV-specific T cell clones of different phenotype may help elucidate the mechanisms of immunotolerance in HB infection.
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PMID:[Preliminary study on HBsAg-specific T cell clones]. 252

Studies were undertaken to evaluate immunomodulating properties of Hepatitis B virus (HBV) preparations: HBsAg, HBeAg and their complexes: HBsAg-IgG and HBeAg-IgG, on PHA-induced lymphocyte proliferation. Cells were obtained from blood of healthy individuals, serologically negative for HBV markers. HBV preparations were purified from sera of children with HBV-mediated glomerulonephritis. Suppression of lymphocyte proliferation observed in the presence of HBsAg and HBsAg-IgG complexes was irreversible. However, the suppressive effect of HBeAg and HBeAg-IgG was abolished when these preparations were removed from the culture. Addition of exogenous interleukin-2/IL-2/reversed only the suppressive effect of HBeAg-IgG which was constantly present in the culture. The inhibition of lymphocyte proliferation correlated well with the decreased level of IL-2 activity in cultures with HBV-preparations. Experiments performed using ultracentrifugation indicated that HBV preparations, especially HBsAg and HBsAg-IgG, may bind to IL-2 and inactivate it in supernatants. The experiments indicate that HBV antigens, as well as other viral products, can inhibit lymphocyte proliferative response to the mitogen. Furthermore, we suggest that this inhibition may occur via suppression of IL-2 synthesis.
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PMID:Effect of HBV antigens and their immune complexes on the PHA induced lymphocyte proliferation. Modulatory influence on interleukin-2 activity. 278 51

This report describes a study of in vitro proliferative and antibody responses to the hepatitis B virus surface antigen (HBsAg) of lymphocytes from chronic HBsAg carriers, subjects with naturally acquired immunity, and responders to the hepatitis B vaccine. Peripheral blood T and B lymphocytes were cultured with a wide range of concentrations of HBsAg (0.025-250 ng/ml). We were unable to detect HBsAg-specific proliferation or antibody synthesis in any of the subject groups studied, despite the use of a range of antigen concentrations, cell ratios and culture periods. The addition of recombinant interleukin 2 (rIL-2) or T cell growth factor at either initiation or day 3 of culture enhanced proliferative responses, but in an antigen-independent manner. In contrast to the proliferation observed following the addition of IL-2, the absence of responses to specific antigen suggest there may be low numbers of HBsAg-specific precursors in the peripheral blood.
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PMID:HBsAg-induced antigen-specific T and B lymphocyte responses in chronic hepatitis B virus carriers and immune individuals. 278 46


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