Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Peripheral blood mononuclear cells and regulatory T cells in acute viral hepatitis. 286 96

Serum beta 2-microglobulin (beta 2m) concentration is increased in pathological processes associated with lymphocyte activation. beta 2m and anti-beta 2m autoantibody (anti-beta 2m) determinations were made in the sera of 41 patients with chronic hepatitis and cirrhosis, respectively, in 19 with systemic lupus erythematosus (SLE) as well as in 27 healthy controls. A pathologically high beta 2m value was found in one-third of inactive persistent hepatitis, and in more than two-thirds of active hepatitis and postnecrotic cirrhosis cases. In SLE it occurred in 16 out of 19 cases. The beta 2m level was elevated mainly in HBV-negative and circulating immune complex-positive hepatic patients. Anti-beta 2m antibody occurred in one-third of chronic hepatitis, but only in one out of 13 cases in cirrhosis and in 12 out of nineteen patients with SLE. The results suggest that beta 2m and anti-beta 2m as in SLE may be further laboratory indicators of immunological activity in inflammatory hepatic disease.
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PMID:Serum beta 2-microglobulin (beta 2m) and anti-beta 2m antibody in chronic hepatitis. 329 46

beta 2-Microglobulin display was examined in 131 liver biopsies from patients with acute and chronic type B hepatitis, using an indirect immunoperoxidase method. Enhanced expression of beta 2-microglobulin on hepatocyte membranes was observed in patients with acute hepatitis, chronic active hepatitis with moderate to severe activity and cirrhosis, when compared with normal liver. In acute hepatitis, beta 2-microglobulin-positive hepatocytes were mainly observed in perivenular areas in association with bridging necrosis. In chronic hepatitis, beta 2-microglobulin-positive hepatocytes were observed mainly in periportal zones and in some areas of lobular activity. Diffuse-enhanced display of beta 2-microglobulin on hepatocytes was observed in 5 of 6 patients treated with lymphoblastoid interferon as part of a trial of antiviral therapy. The mechanism by which beta 2-microglobulin display is enhanced on hepatocytes in patients not treated with interferon is uncertain. However, display of beta 2-microglobulin on hepatocytes probably reflects display of HLA-A, B and C antigens and may influence the course of hepatitis B virus infection by increasing susceptibility of the affected cells to T cell-mediated immune attack.
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PMID:Expression of beta 2-microglobulin on hepatocytes in acute and chronic type B hepatitis. 351 Sep 50

Using antibodies directed to beta 2-microglobulin (b2-m) and HLADR antigens, the expression of MHC products by normal and abnormal bile ducts in 90 paraffin-embedded biopsies showing various liver diseases, was studied. Normal and abnormal bile ducts constantly expressed b2-m. Increased b2-m expression was found in 17/19 PBC, and 4/7 chronic aggressive hepatitis or cirrhosis of viral etiology with hepatitic bile duct lesions. Normal bile ducts failed to express HLADR antigens. Aberrant HLADR display was found in 24/26 PBC and 10/16 chronic aggressive hepatitis or cirrhosis of viral etiology with hepatitic bile duct lesions. It is concluded that the pattern of the major histocompatibility complex (MHC) display does not discriminate between PBC and hepatitic bile duct lesions. Enhanced expression of class I MHC products at the surface of medium-sized bile ducts in PBC may render these structures more susceptible to lysis by cytotoxic T-cells, whereas its significance in chronic aggressive hepatitis or cirrhosis remains unknown. Aberrant expression of HLADR antigens by abnormal bile ducts in PBC and chronic aggressive hepatitis or cirrhosis of viral etiology is probably induced by gamma-interferon, liberated by intra-epithelial lymphocytes, and may serve to enhance the immune response, either by attracting HLADR-restricted cytotoxic T-cells or by the presentation of non-self antigens at the surface of bile duct epithelium.
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PMID:Expression of MHC products by normal and abnormal bile duct epithelium. 354 67

Serum levels of beta 2-microglobulin (beta 2-M) were found to be significantly elevated in acute viral hepatitis, chronic persistent or active hepatitis and liver cirrhosis. beta 2-M values were significantly lower in chronic persistent hepatitis than in the three other groups. Serum beta 2-M was normal in 75 asymptomatic carriers of HBsAg. Steroid therapy was followed by reduction of serum beta 2-M levels in 11 cases of chronic active hepatitis. Variations of beta 2-M were independent from that of transaminases, bilirubin and gamma-globulins.
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PMID:Significance of beta 2-microglobulin in liver diseases. 615 23

The level of tumor markers (alpha-fetoprotein, carcinoembryonic antigen, ferritin, beta 2-microglobulin) in the blood serum was determined in 147 patients with benign and malignant hepatic diseases, 105 patients with cancer of extrahepatic site, Stage I-IV, without liver metastases (a control group) and 36 practically healthy persons. An analysis of the results obtained allowed one to establish that an increase in the concentration of tumor markers as compared to the normal one, is noted in both malignant and benign hepatic diseases as well as in the control group. However hepatic tumors were caused by a more frequent rise of the concentration of tumor markers in the blood serum with higher absolute values. Among benign hepatic diseases the most frequent increase in the level of tumor markers was noted in hepatitis and cirrhosis.
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PMID:[Tumor markers in focal and diffuse liver diseases]. 620 93

T-cell immunity and serum levels of thymosin alpha 1, beta 2-microglobulin, circulating immune complexes, serum immunoglobulin levels, antibodies to hepatitis surface or core antigen, and to cytomegalovirus, and Epstein-Barr virus were investigated in 51 patients with haemophilia A ranging in age from 2 to 52 years. All patients had received commercial U.S. lyophilized concentrates of antihaemophilic factor (AHF). The mean helper/cytotoxic-suppressor (OKT4/OKT8) ratio of 11 pre-adolescents (1.6 +/- 0.4 SE) was not significantly different from that of age matched normal controls. In contrast, the mean OKT4/OKT8 ratios of 13 adolescent (1.2 +/- 0.2 SE) and 23 adult (0.8 +/- 0.1 SE) haemophiliacs were significantly reduced. Abnormalities of lymphocyte mitogenic responses were found only in adult haemophiliacs. Nine individuals treated with commercial U.S. prothrombin complex concentrates for antibodies directed against AHF or for haemophilia B had normal mean OKT4/OKT8 values. The mean serum thymosin alpha 1 levels for each age category was similar to that of age matched controls; however, regression analysis revealed a significant relationship between elevated thymosin alpha 1 levels and decreased OKT4/OKT8 ratios in adult haemophiliacs (P = 0.012). Although the mean serum level of beta 2-microglobulin was significantly increased in the adult haemophiliac group, there was no correlation between OKT4/OKT8 ratios and any of the other serologic parameters studied.
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PMID:Inverse correlation between age related abnormalities of T-cell immunity and circulating thymosin alpha 1 levels in haemophilia A. 623 39

Nonobese diabetic (NOD) mice and beta 2-microglobulin-gene-ablated mice (beta 2M -/-) show impaired presentation of major histocompatibility complex (MHC) class I and self-peptides, structures now recognized as critical for T-cell education to endogenous peptides. The naturally occurring NOD class I presentation abnormality appears to be attributable to, in part, a quantitative defect in the production of Tap-1 mRNA; Tap-1 with Tap-2 normally functions as a transporter for stable self-peptide and class I assembly. This study attempts to reverse NOD and beta 2-M -/- mouse autoreactivity by introduced or reestablished syngeneic class I presentation. Introduction of MHC class I and self-peptides on syngeneic MHC class I-matched cells specifically prevented diabetes in NOD mice and eliminated in vitro class I-directed T-cell autoreactivity in NOD and beta 2M -/- mice. Reestablishment of endogenous class I and self-peptide presentation in NOD mice was achieved with two well-described cures for the NOD mouse, complete Freund's adjuvant and mouse hepatitis virus. Both treatments induced Tap-1 mRNA, reestablished class I presentation of endogenous antigens, and eliminated in vitro and in vivo T-cell autoreactivity of self-peptides in the class I groove. These results substantiate a therapeutic role of self-peptide complexed with class I for T-cell education and suggest that some well-described NOD treatments may work, in part, through reestablishment of tolerance through class I and self-peptide.
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PMID:Elimination of self-peptide major histocompatibility complex class I reactivity in NOD and beta 2-microglobulin-negative mice. 765 37

Serum beta 2-microglobulin concentrations were assayed in 14 patients with acute hepatitis A, 16 with acute hepatitis B and 10 with hepatitis C. Serum samples were taken from each patient in the first and the second week of hospitalization and in the period of aminotransferase normalization. There was a significant increase of beta 2-microglobulin level in every type of hepatitis compared to the control group. A raised serum beta 2-microglobulin concentration persisted during convalescent period. It decreased gradually in type A and B of hepatitis. Serum beta 2-microglobulin level during convalescence in hepatitis C was similar to that of first weeks of hospitalization.
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PMID:[Level of beta 2-microglobulin in serum of patients with acute viral hepatitis types A, B and C]. 892 36

The clinical and pathogenetic importance of a number of features characterizing cell-mediated immunity and nonspecific protective factors in acute virus hepatitis B. 124 patients with hepatitis B virus (HBV) infection were placed under observation. Of these, 115 patients had acute virus hepatitis B, 6 patients had acute virus hepatitis of mixed etiology (B + delta) and 3 patients had chronic virus hepatitis B. The study included, besides the detection of virus hepatitis markers and the biochemical analysis of blood, the determination of subpopulations of peripheral blood lymphocytes (CD3, CD4, CD8, CD57), the functional activity of natural killers, characteristics of the interferon status, serum neopterin and beta 2-microglobulin in blood serum. Considerable changes in cell-mediated immunity and the interferon system were found to occur and the optimum immune response in acute virus hepatitis B was characterized.
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PMID:[The characteristics of the immune response in acute viral hepatitis B]. 908 33


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