concanavalin-a and Hepatitis-B

Roots of Sophora flavescens is an important herbal medicine for treatment of HBV and hepatic carcinoma in China. Alkaloids in the root were well known for exhibiting good hepato-protective and anti-HBV effects. However, polysaccharides as main components in the root remained unknown. In the studies, we investigated the chemical features and hepatoprotective effects of Sophora flavescens polysaccharides (SFP-100 and its active fractions) with ConA-induced hepatitis mice, human liver LO2 cells and HepG2.2.15 cells. The results showed that SFP-100 was composed of arabinose, glucose, galactose and galacturonic acid, SFP-100-A mainly contained glucose. SFP-100-B and SFP-100-C were acidic polysaccharides. SFP-100 significantly decreased hepatocytes apoptosis, inhibited the infiltration of neutrophils and macrophages into liver, and improved the production of IFN-γ and IL-6 of splenocytes in ConA-induced hepatitis mice. SFP-100 and its two sugar fractions increased LO2 cell proliferation and reduced cell apoptosis induced by ConA. SFP-100, SFP-100-A and SFP-100-C remarkedly inhibited the secretion of HBsAg and HBeAg by HepG2.2.15 cells.These results suggested Sophora flavescens polysaccharides exerts significant hepatoprotective and anti-HBV roles, and further is used for treatment of immune-mediated liver disease in the future.

Topics: Animals; Antiviral Agents; Body Weight; Cell Proliferation; Cell Survival; Chemical and Drug Induced Liver Injury; Concanavalin A; Cytokines; Disease Models, Animal; Female; Hepatitis B; Hepatitis B virus; Hepatocytes; Lymphocytes; Mice; Organ Size; Plant Extracts; Plant Roots; Polysaccharides; Protective Agents; Sophora

Hepatitis B virus surface antigen (HBsAg) carriers are highly susceptible to liver injury triggered by environmental biochemical stimulation. Previously, we have reported an inverse correlation between γδ T cells and liver damage in patients with hepatitis B virus (HBV). However, whether γδ T cells play a role in regulating the hypersensitivity of HBsAg carriers to biochemical stimulation-induced hepatitis is unknown. In this study, using HBV transgenic (HBs-Tg) and HBs-Tg T-cell receptor-δ-deficient (TCR-δ

Topics: Animals; Cells, Cultured; Concanavalin A; Hepatitis B; Hepatitis B Surface Antigens; Hepatitis B virus; Humans; Interferon-gamma; Interleukin-17; Interleukin-23; Liver; Mice; Mice, Inbred C57BL; Mice, Knockout; Mice, Transgenic; Necrosis; Receptors, Antigen, T-Cell, gamma-delta; T-Lymphocytes

Infection with hepatitis B virus (HBV) continues to be a major global cause of acute and chronic liver disease with high mortality. Herein, we examined both the anti-HBV and hepatoprotective activity of α-DDB-FNC. In human HBV-transfected liver cell line HepG2.2.15, α-DDB-FNC effectively suppressed the secretion of HBV antigens in a time and dose-dependent manner with 25.11% inhibition on HBeAg and 43.68% on HBsAg at 2.5 μM on day 9. Consistent with the HBV antigen reduction, α-DDB-FNC (2.5 μM) also reduced HBV DNA level by 77.74% extracellularly and 78.94% intracellularly on day 9. In the duck hepatitis B virus (DHBV) infected ducks, after α-DDB-FNC was given once daily for 10 days, the serum and liver DHBV DNA levels were reduced markedly with 96.81% and 97.21% at 10 mgkg(-1) on day 10, respectively. In Con A-induced immunological liver-injury mice, α-DDB-FNC significantly inhibited the elevation of serum ALT, AST, TBiL and liver MDA, NO levels. Furthermore, significant improvement of the liver was observed after α-DDB-FNC treatment both in ducks and mice, as evaluated by the histopathological analysis. In conclusion, our results demonstrated that α-DDB-FNC possesses both antiviral activity against HBV and hepatoprotective effect to Con A-induced liver-injury mice.

Topics: Animals; Antiviral Agents; Benzodioxoles; Cell Survival; Chemical and Drug Induced Liver Injury; Concanavalin A; Cytidine; Cytoprotection; DNA Replication; DNA, Viral; Dose-Response Relationship, Drug; Ducks; Hep G2 Cells; Hepatitis B; Hepatitis B e Antigens; Hepatitis B Surface Antigens; Hepatitis B virus; Humans; Liver; Male; Mice; Time Factors; Virus Replication

Interleukin-22 (IL-22), which acts as either a proinflammatory or anti-inflammatory cytokine in various disease models, is markedly up-regulated in chronic liver diseases, including hepatitis B and C. In this report, we demonstrate a strong correlation between IL-22 expression in the liver with active, inflammatory human liver disease. To clarify the role of IL-22 up-regulation in the pathogenesis of liver diseases, liver-specific IL-22 transgenic (IL-22TG) mice, under the control of albumin promoter, were developed. Despite elevated IL-22 serum levels ranging from 4,000 to 7,000 pg/mL, IL-22TG mice developed normally without obvious adverse phenotypes or evidence of chronic inflammation (except for slightly thicker epidermis and minor inflammation of the skin) compared with wild-type mice. Interestingly, IL-22TG mice were completely resistant to concanavalin A-induced T cell hepatitis with minimal effect on liver inflammation and had accelerated liver regeneration after partial hepatectomy. Although they did not spontaneously develop liver tumors, IL-22TG mice were more susceptible to diethylnitrosamine-induced liver cancer. Microarray analyses revealed that a variety of antioxidant, mitogenic, acute phase genes were up-regulated in the livers of IL-22TG mice compared with those from wild-type mice.. These findings indicate that localized production of IL-22 in the liver promotes hepatocyte survival and proliferation but primes the liver to be more susceptible to tumor development without significantly affecting liver inflammation.

Topics: Animals; Cell Survival; Chemical and Drug Induced Liver Injury, Chronic; Concanavalin A; Diethylnitrosamine; Disease Models, Animal; Disease Progression; Hepatectomy; Hepatitis B; Hepatitis C; Humans; Interleukin-22; Interleukins; Liver; Liver Diseases; Liver Neoplasms; Liver Regeneration; Mice; Mice, Inbred C57BL; Mice, Transgenic

To examine the potential correlation between serum REST corepressor 3 (RCOR3) level and the outcome of patients with hepatitis B.. Concanavalin A (ConA)-induced mouse hepatitis model was used. The mRNA level of RCOR3 in mouse liver was measured using GeneChip array and real-time PCR. One hundred seventy-seven patients with hepatitis B and 34 healthy individuals were categorized into six groups including mild chronic hepatitis, moderate chronic hepatitis B, severe hepatitis B (SHB), cirrhosis, hepatocellular carcinoma (HCC) and healthy control. Serum levels of human RCOR3 were measured using ELISA.. In the mouse hepatitis model, the mRNA level of RCOR3 in liver was reduced early after exposure to ConA, then increased after 6 h of exposure. There was no significant difference in the serum RCOR3 level between the mild chronic hepatitis B and the control groups. The serum RCOR3 level was significantly increased in the moderate chronic hepatitis B group, but significantly reduced in SHB, cirrhosis and HCC groups, as compared with the control group. Moreover, the serum RCOR3 levels in SHB, cirrhosis and liver cancer patients were significantly lower than those in the patients with moderate chronic hepatitis B and with mild chronic hepatitis B. Rank correlation analysis revealed a significant correlation between serum RCOR3 level and total bilirubin (r=-0.305, P<0.01). There was no significant correlation between RCOR3 on one hand, and alanine transaminase (r=0.014, P>0.05) or aspartate transaminase (r=-0.079, P>0.05) on the other hand.. Serum RCOR3 level may reflect the degree of liver damage, which might be a potential biomarker for the outcome of patients with hepatitis B.

Topics: Animals; Co-Repressor Proteins; Concanavalin A; Enzyme-Linked Immunosorbent Assay; Hepatitis B; Humans; Liver; Male; Mice; Mice, Inbred BALB C; Nerve Tissue Proteins; Prognosis; Repressor Proteins; RNA, Messenger

Interleukin 15 (IL-15) is a member of the four-helix bundle cytokine family and has T cell growth factor activity. IL-15 plays a unique role in both innate and adaptive immune cell homeostasis, particularly for the development of NK cells and CD8+memory cells. It may be useful for stimulation of specific immune responses in chronic viral infection such as hepatitis B virus infection. The woodchuck model is an informative animal model for studies on hepadnavirus infection and therapeutic interventions. Here, the complete coding sequence of woodchuck IL-15 (wIL-15) was cloned and sequenced. wIL-15 shows a high homology (>70%) to its counterparts of other mammalian species. His-tagged recombinant wIL-15 protein was expressed and purified and showed the ability to promote the proliferation of activated mouse splenocytes and woodchuck peripheral blood lymphocytes. Further, examination of mRNA amounts in liver samples of woodchucks by semi-quantitative RT-PCR showed a slightly increased expression of wIL-15 in woodchuck livers during chronic woodchuck hepatitis virus infection. This available information will provide a basis for further studies on the function of IL-15 in the context of acute and chronic hepadnavirus infection and its potential therapeutic use for chronic hepatitis B virus infection in the woodchuck model.

Topics: Amino Acid Sequence; Animals; Blotting, Western; Cell Proliferation; Cloning, Molecular; Concanavalin A; DNA, Complementary; Escherichia coli; Gene Expression; Hepatitis B; Hepatitis B Virus, Woodchuck; Interleukin-15; Leukocytes, Mononuclear; Liver; Lymphocyte Activation; Marmota; Molecular Sequence Data; Recombinant Proteins; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Sequence Analysis, DNA; Sequence Homology, Amino Acid; Spleen

Characterization of cellular immune response to antigens of woodchuck hepatitis virus (WHV) can contribute to the understanding of acute resolving and chronic outcome of hepadnavirus infection. Studies were limited because peripheral blood mononuclear cells (PBMCs) of woodchucks failed to incorporate [3H]thymidine sufficiently. Therefore, we established a non-radioactive proliferation assay for woodchuck PBMCs using 5-bromo-2'-deoxyuridine (BrdU) as thymidine analogue. Mitogen- and WHV core protein-(WHcAg) induced PBMC proliferation was detected by BrdU incorporation and compared to an assay using 2[3H]adenine. After stimulation with concanavalin A (ConA) and phytohaemagglutinin (PHA) we observed significant PBMC proliferation with both assays. Mitogen-induced nucleoside uptake of PBMCs into cellular DNA was confirmed by detection of 1',2'[3H]BrdU and 2[3H]adenine in extracted DNA. PBMCs obtained during the acute phase of WHV infection could be stimulated by WHcAg, whereas no WHcAg-induced proliferation of PBMCs was found in WHV-negative animals. PBMCs of chronic WHV carriers showed only a weak response to WHcAg. The established assays will be useful in determining the kinetics of cellular immune responses to different WHV antigens in the course of WHV infection and may provide an insight into mechanisms responsible for chronic outcome of hepadnavirus infection.

Topics: Adenine; Animals; Bromodeoxyuridine; Cell Division; Concanavalin A; DNA; Hepatitis B; Hepatitis B Core Antigens; Hepatitis B Virus, Woodchuck; Isotope Labeling; Leukocytes, Mononuclear; Marmota; Mitogens; Phytohemagglutinins; RNA; Tritium

Patients with hepatitis have multiple immunologic abnormalities, which may be related to cytokine production.. We examined the in vitro production of interleukins (IL-2, IL-4, IL-6), tumor necrosis factor-alpha (TNF-alpha), and interferon-gamma (IFN-gamma) in purified peripheral blood mononuclear cells (PBMCs) of patients with hepatitis B virus positive (HBV), acute viral hepatitis (A-HBV), HBV + chronic active hepatitis (HBV-CAH), and autoimmune-type chronic active hepatitis (AI-ACH).. IFN-gamma and TNF-alpha production were characteristically higher in patients with A-HBV than in healthy control subjects (p < 0.001). However, patients with AI-CAH produced highly elevated levels of IL-4 and IL-6 compared with patients with A-HBV and HBV-CAH and healthy control subjects. The cytokine profile (PBMC-induced IL-2, IL-4, IL-6, IFN-gamma, and TNF-alpha production) is different in A-HBV, HBV-CAH, and AI-CAH disease. The increased cytokine secretion (IFN-gamma and TNF-alpha in A-HBV and IL-4 and IL-6 in AI-CAH) could reflect altered relative frequencies of different cell phenotypes in these diseases.. Specific cytokine production may be important in the pathophysiology associated with diverse inflammatory states in patients with hepatitis.

Topics: Adult; Autoimmune Diseases; Calcimycin; Concanavalin A; Cytokines; Female; Hepatitis B; Hepatitis, Chronic; Humans; In Vitro Techniques; Interferon-gamma; Interleukin-2; Interleukin-4; Interleukin-6; Leukocytes, Mononuclear; Male; Tetradecanoylphorbol Acetate; Tumor Necrosis Factor-alpha

Peripheral blood mononuclear cells (PBMC) from 25 patients with chronic hepatitis B were tested for the presence of free monomeric hepatitis B virus (HBV) DNA migrating as a single 3.2 Kb band by Southern blot analysis. The PBMC were cultured for 7 days in the presence of phytohemagglutinin (PHA) or concanavalin A (ConA) both of which yielded a proliferative response. By contrast, both bacterial lipopolysaccharide (LPS) and interleukin 2 (IL2) failed to do so. Dot blot assays were used to monitor HBV DNA level increase within PBMC. Following mitogen exposure HBV DNA levels increased above pre-stimulation levels in 19/25 PHA cultures, 6/15 ConA cultures, 1/15 LPS cultures, and 1/15 IL2 cultures. In 15 patients, Southern blot analysis was carried out before and after PHA exposure. In 13/15 cases, a single 3.2 Kb band was observed in unstimulated cultures as well as in PHA cultures even though PHA induced a HBV DNA increase. One case exhibited bands migrating faster than the 3.2 Kb signal, compatible with replicating intermediates and one case provided evidence of viral concatemers within PBMC after PHA stimulation. No HBV DNA was detected in the culture supernatants. The increase of HBV DNA level in PBMC induced by mitogen was strongly associated with an increase in HBV DNA expression (HBV RNA and HBs antigen). These studies indicate that HBV DNA present in human PBMC does represent a potential reservoir for infection with endogenous reactivation following PBMC activation.

Topics: Blotting, Southern; Chronic Disease; Concanavalin A; Culture Media; DNA, Viral; Female; Hepatitis B; Hepatitis B Surface Antigens; Hepatitis B virus; Humans; Interleukin-2; Leukocytes, Mononuclear; Lipopolysaccharides; Male; Mitogens; Phytohemagglutinins; RNA, Viral

Serum samples from 20 patients with acute exacerbation of chronic hepatitis due to hepatitis B virus and 20 patients with hepatocellular carcinoma arising from B viral cirrhosis with elevated levels of alpha-fetoprotein (AFP) were analyzed by affinity column chromatography for concanavalin A binding. Serum AFP was tested at regular intervals in all of these patients. Acute exacerbation was defined as elevation of serum transaminase greater than 300 IU/L in patients with chronic hepatitis B. In hepatocellular carcinoma, serum AFP levels fluctuated but remained higher than 92 ng/ml, whereas, in acute exacerbation of chronic hepatitis B, serum AFP levels returned to normal within 3-12 months of follow-up. The results of concanavalin A-binding assay revealed that AFP from both these groups had a high affinity for concanavalin A, and this assay could not be used to discriminate between the two conditions.

Topics: Adult; Aged; alpha-Fetoproteins; Carcinoma, Hepatocellular; Chromatography, Affinity; Chronic Disease; Concanavalin A; Diagnosis, Differential; Female; Follow-Up Studies; Hepatitis B; Humans; Liver Neoplasms; Male; Middle Aged

Suppressor T-cell activity and allogeneic T-cell response to concanavalin A (ConA) were investigated in 46 patients chronically infected with hepatitis B virus (HBV). Thirty-eight patients had chronic active hepatitis, seven of whom were superinfected with Delta virus, and eight were healthy chronic HBV carriers. T-cell suppressor activity was in the normal range in healthy carriers and in patients negative for serum HBV-DNA, independent of the e antigen status. In contrast, the group of patients positive for HBV-DNA exhibited a significant reduction in suppressor activity. Longitudinal studies in patients who cleared serum HBV-DNA demonstrated that suppressor T-cell activity became normal thereafter. These results suggest a relationship between suppressor T-cell function and the stage of viral replication in individuals with chronic HBV infection.

Topics: Adult; Aged; Carrier State; Chronic Disease; Concanavalin A; DNA Replication; DNA, Viral; Female; Hepatitis B; Hepatitis B virus; Hepatitis, Chronic; Humans; Immunity, Cellular; Longitudinal Studies; Lymphocyte Activation; Male; Middle Aged; T-Lymphocytes, Regulatory; Virus Replication

Topics: Adult; Concanavalin A; Female; Hepatitis B; Hepatitis B Antibodies; Hepatitis B Surface Antigens; Hepatitis B Vaccines; Humans; In Vitro Techniques; Interleukin-2; Lymphocyte Activation; Male; Radioimmunoassay; Thymidine; Tritium; Vaccines, Synthetic; Viral Hepatitis Vaccines

To investigate the relationship between liver damage and immune regulation in hepatitis B virus (HBV) infection, 68 patients with HBsAg in serum and a spectrum of liver damage have been studied and compared with 25 controls. In HBsAg carriers, spontaneous IgG production was elevated only in those with chronic active hepatitis (P less than 0.05) whilst those with less severe inflammation had values comparable to normals. Concanavalin A (Con A) induced suppressor cell regulation of IgG producing cells was impaired in those with chronic active hepatitis (P less than 0.01) and those with chronic persistent hepatitis (P = 0.05) and there was a correlation in both groups of patients with the severity of portal tract inflammation (P less than 0.05). In contrast those with minimal liver damage had values in the normal range. Patients presenting with acute hepatitis B also had elevated spontaneous IgG production (P less than 0.01) and impaired Con A induced suppressor cell regulation of IgG production (P less than 0.01). Sequential study of three patients prior to the detection of HBsAg in serum and subsequently during and after acute hepatitis B showed that such abnormalities were transient and closely related to the onset of liver damage.

Topics: Adult; Antibody-Producing Cells; Concanavalin A; Female; Hepatitis B; Hepatitis B Antigens; Hepatitis delta Antigens; Hepatitis, Chronic; Humans; Immunoglobulin G; In Vitro Techniques; Liver; Lymphocyte Activation; Male; Middle Aged; T-Lymphocytes, Regulatory; Time Factors; Transaminases

Topics: Adult; Concanavalin A; Female; Hepatitis B; Hepatitis, Chronic; Humans; Interferon Type I; Interferon-gamma; Male; Newcastle disease virus; T-Lymphocytes

Patients with acute hepatitis B and HBV-induced chronic hepatitis as well as normal control persons participated in the study. Hepatitis patients of both groups have decreased OKT4+/OKT8+T cell ratios due to an percental increase of OKT8+T cells in peripheral blood compared to the data of controls. Lymphocyte cultures of chronic hepatitis patients show reduced DNA synthesis after stimulation by allogeneic non-T cells, PHA, Con A and PWM. PWM-induced immunoglobulin secretion by B cells, determined by means of a reverse haemolytic plaque assay (RHPA) and a solid phase ELISA, showed comparable results in hepatitis B patients and controls. The AMLR, which is thought to reflect an autologous immunoregulatory phenomenon, is slightly impaired in cultures of hepatitis B patients in comparison to controls. Con A-induced suppressor cell activity on T cell reactions is decreased in hepatitis, whereas suppressor cell activity on B cell activation is within the same range as in cultures of controls. It is concluded from these data, that suppressor cell activity on T cell function is impaired in hepatitis B, whereas B cell functions and suppressor cell activity on B cell function are in the normal range. The results with the functional assays and the finding of increased proportions of OKT8+T cells in hepatitis B are considered to reflect properties of different T cell subpopulations, responsible for different immunoregulatory functions.

Topics: Acute Disease; Chronic Disease; Concanavalin A; Hemolytic Plaque Technique; Hepatitis B; Humans; Immunoglobulins; Leukocyte Count; Lymphocyte Activation; Lymphocyte Culture Test, Mixed; T-Lymphocytes; T-Lymphocytes, Regulatory

Topics: Animals; Concanavalin A; Hepatitis B; Hepatitis B e Antigens; Humans; Leukocyte Count; Lymphocyte Activation; Mice; T-Lymphocytes, Regulatory

Topics: Adult; Aged; alpha-Fetoproteins; Chronic Disease; Concanavalin A; Female; Ferritins; Hepatitis B; Humans; Liver Cirrhosis; Liver Cirrhosis, Alcoholic; Liver Diseases; Liver Neoplasms; Male; Middle Aged

Hepatocellular injury in hepatitis B virus infection may be produced by an autoaggressive hepatocytotoxic immune response. To test the hypothesis that acquired suppressor cell defects may participate in such a response, we assessed the functional integrity of 2 suppressor cell populations in patients with type B viral hepatitis. Spontaneous suppression of the 1-way mixed lymphocyte response by radiation-resistant, adherent peripheral blood mononuclear cells decreases during the acute phase of disease, returns towards normal with clinical recovery, but remains depressed in patients with chronic hepatitis. The degree of spontaneous suppressor cell dysfunction correlates inversely with at least 1 biochemical parameter of hepatocellular injury (SGPT). The functional integrity of this suppressor cell fluctuates during chronic hepatitis and may reflect currently undefined biologic variables in this disease. Mitogen-induced suppression on lymphocyte activation by radiation resistant, nonadherent suppressor cells is also depressed in acute and chronic hepatitis, but it does not correlate with biochemical evidence of hepatocellular injury on an individual-patient basis. Documentation of these generalized defects of nonspecific suppressor cell function establishes a basis for the possible existence of specific anomalies of immuno-regulation that may permit the expression of normally suppressed auoaggressive hepatocytotoxic immune mechanisms in viral hepatitis.

Topics: Adult; Alanine Transaminase; Concanavalin A; Female; Hepatitis B; Humans; Lymphocyte Activation; Lymphocyte Culture Test, Mixed; Lymphocytes; Male; T-Lymphocytes; T-Lymphocytes, Regulatory; Time Factors

Topics: Adult; Cell Migration Inhibition; Chronic Disease; Concanavalin A; Hepatitis B; Humans; Leukocytes; Middle Aged

Suppressor cell function was studied in twenty-nine patients with chronic active hepatitis (CAH) in relation to possible aetiological causes and activity of liver disease. All fifteen patients with evidence of viral aetiology (ten HBsAg-positive CAH and five non-A, non-B CAH) showed normal suppressor cell function independently of severity of liver damage. In contrast, fourteen patients with HBsAg-negative CAH, including four cases with circulating antibodies to the hepatitis B virus, demonstrated a significant reduction in supprpessor cell activity compared to control subjects. No significant difference was found in this group between cases with and without circulating autoantibodies. In four out of five HBsAg-negative patients tested serially suppressor cell defect correlated with disease activity suggesting an abnormality in the regulation rather than a depletion of suppressor cells. These results suggest that different mechanisms are responsible for autoimmunity to the liver in virus and non-virus-related CAH.

Topics: Adolescent; Adult; Concanavalin A; Dose-Response Relationship, Drug; Female; Hepatitis; Hepatitis B; Hepatitis, Viral, Human; Humans; Lymphocyte Activation; Male; Middle Aged; T-Lymphocytes, Regulatory

Stable E-rosette forming cells from peripheral blood of patients with acute type B hepatitis and from human thymus were compared with respect to buoyant density and FclgG receptors to stable E-rosette forming lymphocytes generated during culture of normal peripheral blood lymphocytes with concanavalin A. Stable E-rosette forming lymphocytes from patients were distributed in the same high density region of discontinuous bovine serum albumin density gradients as thymus stable E-rosette forming cells but thymus cells did not have FclgG receptors. 5-21% of normal peripheral blood lymphocytes formed stable E-rosettes after culture with concanavalin A but they were found in all densilty fractions. 6-29% of these lymphocytes had receptors for FclgG. The ability to form stable E-rosettes may be a marker for a subset of peripheral blood lymphocytes able to suppress immunological responses.

Topics: Centrifugation, Isopycnic; Concanavalin A; Erythrocytes; Hepatitis B; Humans; Receptors, Fc; Rosette Formation; T-Lymphocytes; Thymus Gland

Con A-Sepharose affinity chromatography may be used in the analysis and classification of immune complexes. Experiments with model immune complexes suggest that the degree of affinity of an immune complex for Con A-Sepharose is determined by the antigen rather than the IgG antibody of the complex. It is possible that partial characterization of unknown antigens linked to IgG in immune complexes may be achieved in many diseases. Preliminary explorations with selected human sera indicate that the IgG containing immune complexes in Burkitt's lymphoma and nasopharyngeal carcinoma have affinity for Con A-Sepharose. By contrast IgG containing immune complexes in chronic hepatitis B seem to lack affinity for Con A-Sepharose.

Topics: Antigen-Antibody Complex; Burkitt Lymphoma; Chromatography, Affinity; Chronic Disease; Concanavalin A; Hepatitis B; Humans; Immune Sera; Immunoglobulin G; Nasopharyngeal Neoplasms; Sepharose

Peripheral lymphocytes from patients with hepatitis-B surface antigen (HBsAg)-positive and -negative acute hepatitis (AH), chronic active hepatitis (CAH), chronic persistent hepatitis (CPH), and normal controls were tested for in vitro cytotoxicity and blast transformation. Cytotoxicity was measured by chrominum (21Cr) release into the medium from 51Cr-labeled Chang liver cells after incubation for 6 h with peripheral lymphocytes at a lymphocyte target cell ratio of 200:1. Concomitant 72-h incubation studies were performed to assess thymus cell-dependent (T) lymphocyte function as measured by conccanavalin A (Con A)- stimulated incorporation of tritiated thymidine (blast transformation) and by cytotoxicity. It was found that (a) lymphocytes from patients with AH are cytotoxic to Chang liver cells compared to controls (P less than 0.001); (b) lymphocytes from patients with acute and chronic hepatitis are less cytotoxic when incubated with autologous and homologous HB2Ag-positive and -negative AH, CAH, and CPH are as cytotoxic as normal controls when stimulated with a nonspecific mitogen such as Con A; and (d) lymphocytes from patients with CAH while on prednisone therapy showed marked depression of cytotoxicity when stimulated with Con A. Thus these studies show that patients with AH have circulating T lymphocytes which are capable of causing the destruction of Chang liver cells. There is no defect in T-cell function as measured by Con A-stimulated cytotoxicity. There is a serum factor (s) in patients with acute and chronic hepatitis which inhibits spontaneous and induced lymphocyte cytotoxicity and blast transformation. Finally, prednisone treatment appears to inhibit lymphocyte cytotoxicity in patients with CAH.

Topics: Acute Disease; Adult; Antibodies, Viral; Antigens, Viral; Bilirubin; Cell Line; Chromium Radioisotopes; Chronic Disease; Concanavalin A; Cytotoxicity Tests, Immunologic; Female; Hepatitis B; Humans; Immune Sera; Immunity, Cellular; Jaundice; Liver; Lymphocyte Activation; Male; Middle Aged; Prednisone; T-Lymphocytes