Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0019163 (
hepatitis B
)
38,309
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
To test the hypothesis that reduced lymphocyte transformation in response to PHA in chronic hepatitis B virus infection might be due to deficient lymphokine production, lymphocyte transformation was measured in the presence or absence of exogenous interleukin 1,
interleukin 2
or both, or, as a source of mixed lymphokines, supernatants from mixed lymphocyte reactions. The response to PHA was significantly impaired in patients compared to controls, but was not corrected by interleukin 1,
interleukin 2
or supernatant from mixed lymphocyte reactions over a wide range of concentrations. Variation of the proportion of monocytes in culture or the addition of indomethacin had no effect on lymphocyte transformation. Thus, reduced lymphocyte proliferation in response to PHA in patients with chronic hepatitis B virus infection cannot be attributed to deficient lymphokine production or to active suppression by monocytes or prostaglandins and a direct role for the
hepatitis B
virus or a viral product is under investigation.
...
PMID:Failure of exogenous interleukin 1 and interleukin 2 to correct decreased lymphocyte transformation in chronic hepatitis B virus carriers. 295 84
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.
...
PMID:In vitro anti-HBs antibody synthesis from anti-hepatitis B vaccine recipients. 296 89
In dialysis patients the immune response to
hepatitis B
-vaccination is greatly impaired. In vitro the non-responders show a failure of the monocytes to support the process of primary T-cell activation. This defect results in a lack of
interleukin 2
-production and an enhanced sensitivity of the interleukin-2 receptor system. Addition of low doses of interleukin-2 fully reconstitutes the deficient immune response in vitro. Furthermore, the local application of low dose interleukin-2 during a standard vaccination with 40 micrograms
hepatitis B
-vaccine normalizes the non-responder state in vivo.
...
PMID:[Secondary immune deficiency in renal failure exemplified by hepatitis B vaccination]. 297 76
The production in vitro of antibody to
hepatitis B
surface antigen by peripheral blood mononuclear cells of healthy volunteers was studied after each of the three doses of
hepatitis B
vaccine. An in vitro
hepatitis B
surface antigen antibody response was successfully induced in 12% of the specimens taken over a 7 month period. The response to this antigen was induced in additional samples if cells had been treated previously with anti-CD4 and complement or anti-CD8 and complement prior to culture initiation. The addition of
interleukin 2
could also induce the formation of antibodies to
hepatitis B
surface antigen. The results suggest that the antibody response to
hepatitis B
surface antigen is complex and varies depending on the individual and time of sampling.
...
PMID:Induction of the in vitro anti-HBs response by hepatitis B surface antigen. 297 20
Interferon-gamma (IFN-gamma) was induced from a human peripheral mononuclear fraction by incubation with a streptococcal preparation stabilized with penicillin G (OK432). This IFN-gamma-producing activity was significantly reduced in patients with chronic hepatitis and hepatocellular carcinoma. In patients with liver cirrhosis it was also reduced but not significantly.
Serum hepatitis
B virus DNA and skin tests for the purified protein derivative of tuberculin, phytohemagglutinin-P and a polysaccharide fraction prepared from streptococcus pyogenes Su strain were determined to have no significant relation to this IFN-gamma-producing activity. Although the addition of
interleukin 2
(
IL-2
) to the culture medium enhanced the IFN-gamma-producing activity, there was no difference in this enhancement between normal control and chronic hepatitis. Therefore reduction of the IFN-gamma-producing activity observed in chronic hepatitis seems to be caused by a decreased number of IFN-gamma-producing activity cells or hypofunction of these cells or both. Since HBeAg became negative in patients whose IFN-gamma-producing activity was increased by the administration of the immunopotentiator OK432 or IFN-beta, the IFN-producing system in the patients with B type hepatitis may contribute to the elimination of HBV. Adenine arabinoside suppressed IFN-gamma-producing activity both in vivo and in vitro.
...
PMID:In vitro interferon producing activity of peripheral mononuclear cells in patients with chronic liver disease. 303 38
We investigated the role of the interferon system in the pathogenesis of chronic liver disease. Interferon-gamma production by peripheral blood mononuclear cells was measured with an ELISA. While concanavalin A-stimulated and recombinant
interleukin 2
-stimulated production of interferon-gamma in patients with chronic active hepatitis and liver cirrhosis was significantly decreased when compared with that of controls (518 +/- 189 and 729 +/- 195 units per ml, mean +/- S.D.), there was also a lot of overlap. Addition of indomethacin to the cultures partially restored interferon-gamma production in patients with chronic active hepatitis and liver cirrhosis, indicating that suppressor function of monocytes was, in part, responsible for the diminished interferon-gamma production. Serial studies showed that interferon-gamma production rose during acute deterioration of illness, during treatment with
interleukin 2
and with the improvement of clinical course. Interferon-gamma production was not different among
hepatitis B
e antigen or antibody positive, and non-A, non-B patients with chronic active hepatitis and liver cirrhosis. Our findings suggest that diminished interferon-gamma production is associated with disease severity in chronic liver disease, irrespective of the
hepatitis B
virus carrier state. It would be interesting to compare the efficacy of treatment with interferon-gamma or interferon-gamma inducers such as
interleukin 2
in chronic hepatitis B patients with and without decreased in vitro interferon-gamma production.
...
PMID:Interferon-gamma production by peripheral blood mononuclear cells of patients with chronic liver disease. 310 84
Peripheral blood mononuclear cells from asymptomatic
hepatitis B
virus (HBV) carriers and healthy controls were incubated with recombinant interleukin 1 (r-IL1) or recombinant
interleukin 2
(r-IL2) at 37 degrees C for 24 hours and with pokeweed mitogen (PWM) and estradiol for 72 hours. The number of antibody-producing cells was counted by hemolytic plaque assay. When the mononuclear cells were not pretreated with r-IL1 or r-IL2, the number of antibody-producing cells was not increased by estradiol in asymptomatic HBV carriers. However, when the mononuclear cells were pretreated with r-IL1 or r-IL2, the number of antibody-producing cells was increased. As we have reported before, this may be have been due to the increase in the estradiol-binding capacity of the mononuclear cells by treatment with IL1 and IL2. In asymptomatic HBv carriers, IL1 and IL2 production of the mononuclear cells or the response of the mononuclear cells to IL1 and IL2 is reduced. Consequently, the estradiol binding capacity is decreased, and antibody production is not increased by estradiol.
...
PMID:Effect of interleukin 1 and interleukin 2 on antibody production in asymptomatic hepatitis B virus (HBV) carriers. 326 Dec 68
Studies were undertaken to determine whether induction of antibody to
hepatitis B
surface antigen (anti-HBs) production by cultured lymphocytes which had been conducted with pokeweed mitogen (PWM) could be replaced by
interleukin 2
(IL 2). In cultures stimulated with purified HBsAg and IL 2, the comparable levels of anti-HBs production to those obtained in cultures stimulated with PWM alone occurred when peripheral blood mononuclear cells (PBMC) from patients positive for serum anti-HBs and recipients of HBsAg vaccine were used as effector cells. Detectable amounts of anti-HBs were produced only when IL 2 was added to the second-set cultures again. IL 2 or HBsAg alone, however, did not induce anti-HBs production. Anti-HBs production was not observed by the additions of these additives when PBMC from chronic HBsAg carriers and control individuals were used. These findings indicate that IL 2 could modulate the immune response to HBsAg.
...
PMID:Enhancement of antibody production to hepatitis B surface antigen by interleukin 2. 326 6
Five patients with HBe antigen-positive chronic active hepatitis were treated with recombinant
interleukin 2
(r-IL2) for 3 to 4 wk. r-IL2 inhibited HBV replication during therapy as judged by decrease of serum DNA polymerase activity. Two of five patients lost HBeAg from serum. Furthermore, characteristic increases of serum aminotransferase were observed during r-IL2 therapy. This rise might have been mediated by enhanced immune responses to
hepatitis B
virus and increased rate of lysis of the infected hepatocytes. No consistent changes in immune markers such as OKT4 positive cells or OKT8 positive cells were demonstrated during or after the therapy. The activities of natural killer cells gradually increased during therapy, although they tended to decrease within 1 wk after the start of r-IL2 injections. In two responders who lost HBeAg from serum, the natural killer activity was high before the therapy, compared with nonresponders. Furthermore, the percentage of OKT4-positive cells in the responders was increased within 1 to 2 wk after starting r-IL2 injections. These findings suggest that the responders might be immunologically different from the nonresponders. Recombinant-IL2 therapy over short periods did not result in complete clearance of
hepatitis B
virus. Further studies with high doses of r-IL2 given over longer periods are warranted.
...
PMID:Effects of human recombinant interleukin 2 in patients with chronic hepatitis B: a preliminary report. 349 71
We investigated impaired cellular immune responses of individuals on chronic hemodialysis by using monoclonal antibodies that trigger differential pathways of T cell activation. Reduced cellular reactivity, which exists in a high proportion of such patients, can be attributed to a failure of the monocyte population to support the process of primary T cell activation in vitro. This defect results in a lack of
interleukin 2
production, which is critically dependent on a monocyte-derived signal. In contrast, T lymphocyte function was found to be physiologic. Perhaps more important, the degree of monocyte dysfunction in vitro correlated with the same patients' in vivo responses to
hepatitis B
vaccination. Addition of recombinant human interleukin 2 fully reconstituted their deficient immune response in vitro.
...
PMID:Selective blockade of the antigen-receptor-mediated pathway of T cell activation in patients with impaired primary immune responses. 349 50
<< Previous
1
2
3
4
Next >>