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

A subpopulation of peripheral blood lymphocytes with the ability to lyse target cells coated with specific antibody (antibody-dependent cell-mediated cytotoxicity, ADCC) was serially studied in a patient with hepatitis B antigen-associated periarteritis nodosa. The effector lymphocytes possess FC and complement receptors but do not require complement for functional activity. We found that the patient's ADCC was decreased during periods of disease activity and was almost normal during remission. The patient's serum could block ADCC in normal lymphocytes, and the blocking ability correlated with the concentration of immune complexes as determined by the Raji cell assay (a radioimmunoassay using complement receptors on human cultured lymphoblastoid cells). The concentration of immune complexes and the ADCC blocking ability of ther serum both correlated with disease activity. Serum from five other patients with active vasculitis was found to contain significant amounts of immune complexes and was able to block normal ADCC. It appears that the ADCC assay can be used to detect the presence of circulating immune complexes and to monitor disease activity in periarteritis nodosa.
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PMID:Immune complexes in hepatitis B antigen-associated periarteritis nodosa. Detection by antibody-dependent cell-mediated cytotoxicity and the Raji cell assay. 1 90

A sensitivie and simple procedure for the detection and quantitation of soluble complement (C)- fixing immune complexes in sera of patients with various disease states has been developed by utilizing C receptors on Raji cells. These cells lack membrane-bound immunoglobulin but have receptors for IgG Fc, C3b, C3d, and possibly with other C proteins. Uptake experiments showed that both aggregated human gamma globulin (AHG) and 7S IgG bound to receptors for IgG Fc; however, AHG reacted with C bound to cells only via receptors for C and this binding was much more efficient than via IgG Fc receptors. AHG was used as an in vitro model of human immune complexes and its uptake by Raji cells was quantitated by 125I-radiolabeled antihuman IgG. The limit of sensitivity of this test was 6 mug AHG/ml serum. The ability of Raji cells to detect AHG in serum depended on the amount of radioactive antibody used and the size of aggregates. The presence of an excess of C somewhat inhibited binding of AHG containing C to Raji cells. The efficient binding of AHG by receptors for C on Raji cells was used for the detection and quantitation of immune complexes in human sera. Raji cells were incubated with sera to be tested and then reacted with excess radiolabeled antihuman IgG; the amount of radioactivity bound to the washed cells was determined and referred to a standard curve of radioactive antibody uptake by cells previously incubated with increasing amounts of AHG in serum. Thereby immune complexes were detected and quantitated in serum hepatitis, systemic lupus erythematosus, vasculitis, subacute sclerosing panencephalitis, dengue hemorrhagic fever, and malignancies.
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PMID:The Raji cell radioimmune assay for detecting immune complexes in human sera. 12 62

A case of chronic polyneuropathy associated with chronic type B hepatitis was described. A 31 year-old male was admitted to our hospital with a 2-year history of progressive weakness and sensory disturbances of all limbs. There was past history of acute type B post-transfusion hepatitis after subtotal gastrectomy. On examination there was generalized muscle weakness, particularly in movements of the hands and feet with areflexia. He had a steppage gait. Sensory examination revealed moderately decreased pinprick, light touch, vibration and position sense in the distal portion of all extremities. On admission, hepatitis associated antigen and antibody were negative and positive, respectively. The level of circulating immune complexes was high with the titer of 6.6 micrograms/ml by Clq assay and 16X by Raji cell assay. Liver biopsy revealed fibrosis and periportal inflammatory infiltrate compatible with the diagnosis of chronic viral hepatitis. Sural nerve biopsy showed marked loss of large myelinated fibers and epineural vasculitis with the thickened blood vessel wall and mononuclear cell infiltrates. There have been increasing evidences that extrahepatic manifestations are caused by vasculitis due to HBs antigen-antibody immune complex deposits. On the basis of findings in the literature it seems possible that chronic polyneuropathy may be related to the vasculitis due to HBs antigen-antibody complex deposits after hepatitis B virus infection.
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PMID:[A case of chronic polyneuropathy associated with chronic type B hepatitis]. 317 85

Although it is generally considered that vasculitis of the polyarteritis nodosa (PAN) group and Wegener's granulomatosis (WG) is immune complex (IC) mediated, there are no simultaneous data on circulating IC, complement levels and deposits of Ig and complement in the kidney. Therefore we have performed a retrospective study of 43 patients suffering from PAN and WG. Ig glomerular deposits were uncommon and scanty, except in two patients with WG; C3 deposits were detected in 12 patients, whereas fibrinogen was constantly found when lesions were recent and active. Similar data were obtained for the renal vessel walls. Contrasting with these results, rheumatoid factors and cryoglobulins, suggestive of the presence of circulating IC, were detected respectively in nine of 39 and seven of 37 patients, and IC 'activity' assessed by the Raji cell assay and the Clq binding assay was found respectively in six of 17 and nine of 10 patients before treatment, and in none of 10 and five of seven patients in remission. Haemolytic complement activity and complement components were never decreased, but the C3d breakdown product of C3 was elevated in all the eight patients studied before treatment. Signs of persistent hepatitis B virus (HBV) infection were detected in five of 25 patients of the PAN group, whereas three of eight patients with WG had only anti-HBV antibodies. Furthermore, cytomegalovirus (CMV) could be isolated from the blood in a case of WG before the treatment was started. Persistent interferonaemia was detected in one of five patients. These results suggest either that renal deposition of CIC is transient, the paucity of Ig deposits being due to rapid clearance of IC by phagocytic cells; or alternatively that vascular and glomerular lesions are not caused by CIC, as in some cases of experimental vasculitis induced by infectious agents.
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PMID:Immunopathological studies of polyarteritis nodosa and Wegener's granulomatosis: a report of 43 patients with 51 renal biopsies. 619 53

Using molecular cloning techniques, we constructed and transfected human interleukin-2 gene expressive retroviral vector into a packaging cell line PA317. Geneticin resistant cell clones were identified and pseudoviral particles titred as 3.75 x 10(6)CFU/ml in their culture supernatants. Human interleukin-2 expression level was 5.71IU/ml for NIH3T3, 6IU/ml for both 2. 2. 15 and peripheral blood mononuclear cells after infection with pseudoviral particles with 8 of multiplicity of infection (M. O. I). Low level interleukin-2 expression potentially inhibited hepatitis B virus surface antigens expression of 2. 2. 15 cell line and enhanced cytotoxicity of peripheral blood mononuclear cells against K562 and Raji as target cells, but neither pseudoviral particles without interleukin-2 cDNA nor reccombinant interleukin-2 at 6 IU/ml. These results indicated that retroviral vector-packaging cell line can efficiently transfer and express interleukin-2 cDNA in human somatic cells and low level expression of interleukin-2 potentially inhibits hepatitis B virus surface antigens expression and enhances LAK activity of peripheral blood mononuclear cells of normal persons.
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PMID:[Human interleukin-2 gene transfer and expression inhibits hepatitis B virus surface antigen expression and enhances LAK activity of peripheral blood mononuclear cells of normal adults]. 755 54

A mammalian protein called RFX or NF-X binds to the X box (or X1 box) in the promoters of a number of major histocompatibility (MHC) class II genes. In this study, RFX was shown to have the same DNA-binding specificity as methylated DNA-binding protein (MDBP), and its own cDNA was found to contain a binding site for MDBP in the leader region. MDBP is a ubiquitous mammalian protein that binds to certain DNA sequences preferentially when they are CpG methylated and to other related sequences, like the X box, irrespective of DNA methylation. MDBP from HeLa and Raji cells formed DNA-protein complexes with X-box oligonucleotides that coelectrophoresed with those containing standard MDBP sites. Furthermore, MDBP and X-box oligonucleotides cross-competed for the formation of these DNA-protein complexes. DNA-protein complexes obtained with MDBP sites displayed the same partial supershifting with an antiserum directed to the N terminus of RFX seen for complexes containing an X-box oligonucleotide. Also, the in vitro-transcribed-translated product of a recombinant RFX cDNA bound specifically to MDBP ligands and displayed the DNA methylation-dependent binding of MDBP. RFX therefore contains MDBP activity and thereby also EF-C, EP, and MIF activities that are indistinguishable from MDBP and that bind to methylation-independent sites in the transcriptional enhancers of polyomavirus and hepatitis B virus and to an intron of c-myc.
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PMID:The major histocompatibility complex class II promoter-binding protein RFX (NF-X) is a methylated DNA-binding protein. 841 74

Hepatitis B virus (HBV) is a DNA virus that infects the liver as primary target. Currently, a high affinity receptor for HBV is still unknown. The dendritic cell specific C-type lectin DC-SIGN is involved in pathogen recognition through mannose and fucose containing carbohydrates leading to the induction of an anti-viral immune response. Many glycosylated viruses subvert this immune surveillance function and exploit DC-SIGN as a port of entry and for trans-infection of target cells. The glycosylation pattern on HBV surface antigens (HBsAg) together with the tissue distribution of HBV would allow interaction between HBV and DC-SIGN and its liver-expressed homologue L-SIGN. Therefore, a detailed study to investigate the binding of HBV to DC-SIGN and L-SIGN was performed. For HCV, both DC-SIGN and L-SIGN are known to bind envelope glycoproteins E1 and E2. Soluble DC-SIGN and L-SIGN specifically bound HCV virus-like particles, but no interaction with either HBsAg or HepG2.2.15-derived HBV was detected. Also, neither DC-SIGN nor L-SIGN transfected Raji cells bound HBsAg. In contrast, highly mannosylated HBV, obtained by treating HBV producing HepG2.2.15 cells with the alpha-mannosidase I inhibitor kifunensine, is recognized by DC-SIGN. The alpha-mannosidase I trimming of N-linked oligosaccharide structures thus prevents recognition by DC-SIGN. On the basis of these findings, it is tempting to speculate that HBV exploits mannose trimming as a way to escape recognition by DC-SIGN and thereby subvert a possible immune activation response.
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PMID:Branched oligosaccharide structures on HBV prevent interaction with both DC-SIGN and L-SIGN. 1848 82