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Biomedical subjects

V Barnaba

Publications and source records attributed to V Barnaba.

At least 73 records · Page 4Linked to original sources
PubMed1987

In vitro anti-HBs antibody synthesis from anti-hepatitis B vaccine recipients.

Peripheral blood mononuclear cells (PBMC) from 'responders' recently boosted with hepatitis B vaccine, were studied for synthesis in vitro of antibody to hepatitis B surface antigen (anti-HBs Ab) when stimulated with pokeweed mitogen (PWM) or HBsAg. HBsAg alone can induce an antigen-specific anti-HBs Ab response in vitro; this antibody synthesis is T cell-dependent. In some responders both allogeneic T4+ cells (in absence of PWM or HBsAg) and mixed leucocyte culture supernatants (MLC/SN) (without T cells and antigen) can help responder B cells to produce anti-HBs Ab. Thus, in some immunized subjects, B lymphocytes involved in anti-HBs Ab synthesis are in an advanced phase of differentiation and require only non-antigen specific T cell signals (B cell growth factor or B cell differentiation factor or interleukin 2, etc) to differentiate into antibody-secreting cells. Moreover, the concentration of the antigen necessary to suppress anti-HBs Ab production induced by HBsAg was five times lower than that necessary to suppress antibody production induced by PWM. T cell help for antigen induced anti-HBs Ab could be different from T cell help for the PWM-induced anti-HBs Ab response. Moreover, the finding that the low HBsAg doses inhibiting specific response did not affect the PWM-driven anti-HBs response suggests that antigen-specific T suppressor cells could play a role in this context.

B-Lymphocytes↗
PubMed1987

"Anti-Ia reactivity in sera from patients with chronic active hepatitis (CAH)".

Anti-Ia reactivity in sera from patients with chronic active hepatitis (CAH) were characterized by determining cross-reacting specificities with the antigen defined by anti-Ia monoclonal antibody (MoAb) and by studying the effect of CAH sera on the autologous mixed leukocyte reaction (MLR). Preincubation with autoimmune CAH sera lowered the percentage of Ia+ non-T cells stained by anti-Ia MoAb. HBsAg+ve/HBeAg+ve sera did not exert any blocking activity while 4 out of 11 HBsAg+ve/anti-HBe+ve sera exerted a significant blocking effect. Preincubation of cells with normal human serum (NHS) plus aggregated IgG did not block the binding of MoAb anti-Ia. Sera from patients with autoimmune or HBsAg+ve/anti-HBe+ve CAH, that blocked the binding of anti-Ia MoAb to Ia positive target cells by more than 20%, clearly inhibited the autologous mixed lymphocyte reaction (MLR). Both IgG and IgM fractions obtained by affinity chromatography from CAH sera inhibited the autologous MLR and blocked the binding of anti-Ia antibody to Ia positive target cells. A significant positive correlation (p less than 0.001) between serum anti-Ia reactivity and serum liver membrane antibodies (LMA) was observed. In 4 "autoimmune" CAH patients, steroid treatment induced a dramatic decrease in the anti-Ia reactivity.

Antigen-Antibody Reactions↗
PubMed1986

Effect of 28 consecutive days lymphoblastoid interferon (alpha-IFN) administration on hepatitis B virus related chronic liver disease.

Eight HBsAg, HBeAg, DNA-p, HBV-DNA-positive patients with biopsy-proven chronic hepatitis were treated with human lymphoblastoid interferon (Wellferon) given for 28 consecutive days at a dosage ranging from 2.5 to 7.5 MU/m2 i.m.; 10 patients were used as controls. Our results suggest that certain chronic carriers may respond to the treatment with this agent. In fact, the treated patients showed a permanent inhibition of HBV replication sooner and in higher percentage with respect to untreated patients (37.5% vs 20%). IFN administration does not induce any important changes in the immunoregulatory wetwork, but is able to increase significantly the cytolytic activity of NK cells in the patients who respond to the therapy with a permanent inhibition of HBV replication.

Adult↗
PubMed1986

Characterization of effector cells in lymphocytotoxicity to autologous hepatocytes in HBsAg-positive and autoimmune chronic active hepatitis (CAH).

Peripheral blood lymphocyte subsets involved in cytotoxicity to autologous hepatocytes have been characterized by isolation on antibody-coated Petri dishes in autoimmune and HBsAg-positive chronic active hepatitis (CAH). In autoimmune CAH and in HBsAg-positive CAH without HBcAg in liver tissue, cytotoxicity is sustained by non-T lymphocytes and is confined to M1-positive cells bearing Fc receptors: M1 cytotoxicity inhibition by adding aggregated IgG suggests that these cells are responsible for an antibody-dependent cell-mediated mechanism (ADCC). Moreover, when T-enriched fractions were separated in T4, T8 and 5/9 positive subsets, only the first one showed a significant cytotoxicity: T4 positive cells might act as cytotoxic T cells or might be involved in delayed type hypersensitivity (DTH) reactions. Cytotoxic T lymphocytes in HBsAg-positive CAH with HBcAg in liver tissue are confined in T8 positive subset, while helper/inducer T cells (T4 positive or 5/9 positive) seem to play an important role only in the induction of cell-mediated injury against hepatocytes. The inhibition of T cell-cytotoxicity by preincubating liver cells with monoclonal antibody (Mab) anti-HLA AB and not with Mab anti-HLA DR or aggregated IgG supports the involvement of the class I major histocompatibility complex (MHC) expressed on the hepatocyte surface.

Antibodies, Monoclonal↗
PubMed1985

T-cell subsets in the hyporesponsiveness to hepatitis B surface antigen (HBsAg) and antigen-specific suppressor lymphocytes in chronic hepatitis B virus (HBV) infection.

In contrast to convalescent hepatitis B patients, who exhibit the ability to elicit a specific immune response to HBsAg, patients with chronic hepatitis B virus (HBV) infection are markedly hyporesponsive to HBsAg and show a decrease in the normal ratio of OKT4-positive (helper/inducer) to OKT8-positive (suppressor/cytotoxic) lymphocytes. In this study the role of OKT4-positive and OKT8-positive cells on cellular immune response to HBsAg was evaluated in patients with chronic HBV infection and the ability of such patients to develop antigen-specific suppressor lymphocytes after in vitro sensitization to HBsAg. Elimination of OKT8-positive cells markedly improved the in vitro lymphocyte proliferative response to HBsAg without altering the reactivity of cells from the same donor to PPD or Candida. In contrast, the degree of responsiveness to HBsAg was not affected by the depletion of OKT4-positive cells. In vitro co-culture experiments, performed in the seven chronically HBV-infected patients who showed a proliferative response when their PBM were cultured with purified HBsAg or PPD, have demonstrated that lymphocytes from chronic HBV carriers, stimulated with HBsAg, inhibit the response of autologous PBM to HBsAg but not to the unrelated antigen PPD.

Antibodies, Monoclonal↗
PubMed1985

Peripheral blood mononuclear cells and regulatory T cells in acute viral hepatitis.

During acute viral hepatitis, we observed a significant decrease in OKT4/OKT8 ratio with a significant increase in the OKT8 positive subset in acute type B and non-A-non-B hepatitis. This altered ratio persisted in type B for a long time until HBsAg antibody became detectable, while it soon returned to normal in type A and non-A-non-B hepatitis. In the majority of acute hepatitis the altered ratio is because of an increase and not to a decrease in the whole T cell population, as described in chronic HBV infection. The number of HNK-1 positive cells remained raised during the recovery phase of type B and non-A-non-B hepatitis, a finding consistent with the hypothesis that NK cells play a role in the host defence against B and non-A-non-B virus infections. Serum beta 2-microglobulin concentrations were increased only in acute hepatitis B and non-A-non-B where immunological mechanisms are suspected to be involved, and showed a good correlation with the population of activated OKIa positive cells.

Adolescent↗
PubMed1985

Suppressor T cells role in the unresponsiveness to Candida albicans in chronic mucocutaneous candidiasis.

We investigated the immune function of two members of the same family, mother and son, affected by chronic mucocutaneous candidiasis (CMC). In these cases CMC was not associated with hypofunction of endocrine organs, while the son showed histological feature of chronic active hepatitis. We observed a decrease in OKT4/OKT8 ratio and an increased suppressor cell function in both patients. Elimination of cytotoxic/suppressor T cells by lysis of these cells with OKT8 plus complement markedly improved lymphocyte proliferative responses to Candida antigens but not to unrelated antigens. These data suggest that specific suppression is probably responsible for failure of Candida albicans clearance in CMC patients.

Adolescent↗
PubMed1985

Antigen specific suppressor T cells from chronic hepatitis B virus (HBV) carriers inhibit the responsiveness to HBsAg of allogeneic high-responder lymphocytes.

Immunoregulatory mechanisms in chronic HBsAg carriers have been investigated through the study of in vitro proliferative responses to HBsAg by allogeneic coculture experiments between T lymphocytes from HBsAg + chronic active hepatitis (CAH) patients (HBsAg no responder) and PBMC from subjects boosted with anti-hepatitis B vaccine (high responder). When high-responder PBMC have been challenged with the hepatitis B surface antigen (HBsAg) in the presence of HBsAg no-responder T lymphocytes, HBsAg no-responder T lymphocytes caused an antigen specific, dose-dependent, suppression of the responsiveness of high-responder PBMC. On the other hand, T cells from patients with autoimmune CAH did not exert any suppressor effect in our system. The suppressor T lymphocytes were mitomycin C resistant and were positive for OKT8, but were negative for OKT4. When T8 + cells were depleted from HBsAg no-responder PBMC, the in vitro immunoproliferative response to HBsAg in chronically HBV infected patients was markedly improved. Out data clearly demonstrate the existence of T8 + suppressor T lymphocytes that can control low responsiveness to HBsAg in chronic HBV patients.

Autoimmune Diseases↗
PubMed1985

Immunoregulation of the in vitro anti-HBs antibody synthesis in chronic HBsAg carriers and in recently boosted anti-hepatitis B vaccine recipients.

We report a study on immunoregulation of in vitro antibody to hepatitis B surface antigen (anti-HBs) synthesis induced by pokeweed mitogen (PWM) from peripheral blood mononuclear cells (PBMC) in chronic hepatitis B surface antigen (HBsAg) carriers and in 'high responders', (anti-HBs RIA ratio greater than or equal to 20 in serum), recently boosted with anti-hepatitis B vaccine. Anti-HBs was detected in 11 days PBMC supernatants (SN) from 24 out of 36 'high responders', but in none from 31 chronic HBsAg carriers, despite detectable amounts of polyclonal IgG and antibody to hepatitis B core antigen (anti-HBc) were produced. The lack of anti-HBs production by chronic HBsAg carriers did not seem to be determined by suppressor influences because T lymphocytes from the majority of chronic HBsAg carriers, co-cultured with 'high responders' PBMC did not suppress anti-HBs production. Co-cultures between HBsAg carriers T4 positive (helper/inducer) cells and allogenic 'high responder' non-T cells produced anti-HBs antibody, indicating that HBsAg carrier T cells are not deficient in this allogenic helper function under PWM stimulation. Allogenic cocultures between HBsAg carrier non-T cells and 'high responder' T4 positive cells failed in anti-HBs production: a specific B lymphocyte defect might be involved in the lacking anti-HBs synthesis in chronic HBV patients. Antigen-induced specific anti-HBs synthesis experiments indicate that B cells themselves seem to be the target for HBsAg-induced suppression of anti-HBs antibody response.

Adolescent↗
PubMed1985

Monitoring of NK-1 and NK-15 subsets and natural killer activity in kidney transplant recipients receiving cyclosporine.

NK-1, NK-15 subsets and natural killer (NK) activity were studied in 13 patients, before undergoing renal transplantation and in the post-transplant period. Pretransplant there was a significant reduction of NK activity with a defect in Vmax capacity in all patients. NK-1+ and NK-15+ cell number was normal or slightly increased in all subjects. Post-transplant evaluation under cyclosporine immunosuppression showed a quantitative reduction in NK cells while no changes in NK activity and killing activity have been seen. We conclude that in spite of a numerical decrease, NK activity was not affected by cyclosporine treatment.

Adolescent↗
PubMed1984

Circulating HBsAg/IgM complexes in acute and chronic hepatitis B.

Complexes between HBsAg and IgM have recently been described in the sera of HBsAg carriers. A solid phase RIA for HBsAg/IgM complexes has been described. Fifteen patients with acute viral hepatitis type B, and 52 HBsAg chronic carriers were studied. Testing of serial sera in acute hepatitis patients revealed that HBsAg/IgM complexes disappeared (preceding HBsAg negativization and usually at the same time as seroconversion from "e" to "anti-e") with 4 weeks in all but one patient who became a chronic HBsAg carrier. In addition, HBsAg/IgM complexes were found in 48% of HBsAg chronic carriers, in 69% of CPH patients, but in only 20% of healthy carriers (p less than 0.005). Although complexes were detectable in 93% HBeAg positive chronic carriers, they were also frequently found in anti-HBe positive patients, but never in e/anti-e negative patients (p less than 0.001). HBsAg/IgM complexes seem to be of important prognostic and diagnostic value in acute and chronic hepatitis B.

Antigen-Antibody Complex↗
PubMed1983

Immunoregulatory T cells in HBV-induced chronic liver disease as defined by monoclonal antibodies.

Peripheral blood T lymphocytes and T-cell subsets were analyzed in 19 patients with HBV-associated chronic liver disease, in 9 "autoimmune" chronic active hepatitis patients, and in three patients with HBV acute hepatitis. The percentages of the different T-cell subpopulations were defined by indirect immunofluorescence using monoclonal antibodies against all peripheral blood T cells (OKT3), T helper cells (OKT4), T suppressor cytotoxic cells (OKT8), and Ia antigens (OKIa1). The OKT4/OKT8 ratio was significantly lower in HBsAg+ chronic liver disease patients as compared with controls (P less than 0.001), with both decreases of T helper cells and increases of T suppressor cells, while "autoimmune" chronic active hepatitis patients showed a significantly increased ratio (P less than 0.001). Acute HBV infection was associated with a reversal in the normal ratio of helper to suppressor T lymphocytes. During convalescence helper T lymphocytes increased and suppressor T lymphocytes decreased.

Antibodies, Monoclonal↗
PubMed1983

Relationship between T cell subsets and suppressor cell activity in chronic hepatitis B virus (HBV) infection.

The relationship between T cell subset, as defined by monoclonal antibodies, and suppressor cell function, using a short lived suppressor cell assay, was studied in 38 chronic hepatitis B virus (HBV) carriers and in 32 patients with HBsAg negative chronic active hepatitis (CAH). Patients with HBV chronic infection showed an absolute reduction in the OKT4 positive subset and a significantly decreased OKT4/OKT8 ratio, as compared with healthy controls. Patients with anti-nuclear antibodies (ANA) and anti-smooth muscle antibodies (ASMA) positive CAH with or without antibodies to HBV antigens, namely anti-HBs and anti-HBc, demonstrated a significant reduction in cytotoxic/suppressor T cells and an increased helper/suppressor ratio. A negative correlation between suppressor index (SI) and OKT4/OKT8 ratio (P less than 0.01), and a positive correlation between SI and OKT8 positive cells absolute number (P less than 0.01) were also observed.

Antibodies, Antinuclear↗
PubMed1983

HBeAg/anti-HBe system and development of primary hepatocellular carcinoma in patients with HBsAg-positive liver cirrhosis.

The significance of the HBeAg/anti-HBe system and other HBV markers in the evolution of HBsAg-positive liver cirrhosis to primary hepato-cellular carcinoma (PHC) was studied by following up 70 cirrhotic patients from February 1978 to February 1981. Eight out of 19 (42.1%) patients with HBsAg positive liver cirrhosis developed PHC. On the other hand, only 7.8% of the patients with HBsAg-negative liver cirrhosis developed PHC. In the HBsAg-positive group only the patients who had already seroconverted to anti-HBe (7 out of 11) or were negative for both HBeAg and anti-HBe (1 out of 3) at the time of first observation and showed a histological picture of inactive cirrhosis, developed PHC during the follow-up period. No HBeAg-positive cirrhosis showed such an evolution. The absence of HBeAg in the sera of patients who developed PHC suggests that active HBV replication becomes increasingly defective during the course of malignant transformation.

Antibodies, Viral↗