C4B*Q0 allotype as risk factor for myocardial infarction.
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Adult↗
Biomedical subjects
N Anh-Tuan
Publications and source records attributed to N Anh-Tuan.
HLA-DR1 is associated with vitiligo.
In Eastern Hungary, vitiligo is found to be associated with HLA-DR1. When other autoimmune disorders are also present, DR3 is also increased.
Autoimmune Diseases↗
Effect of conditioned media of acute myeloid leukemia blast cells on complement synthesis by cultured human cells of monocyte and hepatocyte origin.
The effect of conditioned media of 3-day cultures of blast cells from peripheral blood of 5 patients with acute myeloid leukemia (CM-AML) was studied on the synthesis of C2, factor B (Bf) and C1 esterase inhibitor (C1-INH) by human monocyte-macrophage cultures and HepG2 hepatoma cell line. The level of C2 in the culture supernatants was measured by immune hemolysis, those of Bf and C1-INH by ELISA. CM-AML was added to the monocyte cultures on day 3 and replaced by culture fluid on day 6. Compared to the control cultures, CM-AML significantly increased C2 and Bf levels and slightly decreased C1-INH levels in the culture fluids on day 6. On day 9, Bf synthesis enhancement still could be observed but C2 and C1-INH levels did not significantly differ from those of the control. CM-AML significantly increased the synthesis of factor B by the HepG2 cells too. A strong correlation was found between the results of the Bf protein and RNA determinations, which means that the supernatants of AML blasts affect the gene expression of factor B at a pretranslational level. The selective complement synthesis modifying effect of CM-AML was not due to interferons (IFN) because neither IFN-alpha nor IFN-gamma could be detected in these conditioned media. The present findings indicate that the hypercomplementemia observed in AML patients can be due to unknown factor(s) produced by leukemic blast cells.
Blood Cells↗
Gangliosides in acute myeloid leukaemia (AML) and non-Hodgkin's lymphoma (NHL).
Gangliosides of human acute myelomonocytic leukaemia (AMMoL), acute monocytic leukaemia (AMoL) and lymphoblastoid (pre-B) lymphoma cells were analysed by overpressured thin-layer chromatography (OPTLC) followed by scanning densitometry. AMMoL cells were found to contain four gangliosides, viz. GM3 (47.2%), GM1 (31.8%), GD1a (7.5%) and an unidentified compound migrating between GM1 and GD1a (13.5%). In AMoL cells, six components were identified (GM3:51.3%, GM1:13.4%, GD3:7.8%, GD1a:4.7%, GD1b:6%, and an unidentified compound migrating between GM2 and GM1). The total gangliosides extracted from pre-B lymphoma cells of the hand-mirror variant were composed of 10 species (GM3:50.8%, GM2:11.2%, GM1:7.8%, GD3:2.3%, GD1a:1.1%, GD1b:2.2%, GT1:1.6%, and three unidentified components with chromatographic mobilities between GM2 and GD1a). Additional studies must still be performed to clarify the question as to whether ganglioside GD3 represent a qualitative glycolipid marker for AMoL and pre-B lymphoblastic lymphoma.
Chromatography, Thin Layer↗
Ganglioside composition in common acute lymphoblastic leukaemia.
Human leukaemic lymphocytes of the common acute lymphoblastic leukaemia (cALL) subtype were analysed for ganglioside composition by over pressured layer chromatography-densitometry. Two major ganglioside components, GM3 (58.0-77.8% of the total sialic acid content) and GM1 (20.7%-29.2%), and some minor compounds, GM2 (trace amounts to 9.6%) and unidentified gangliosides with chromatographic mobility between GM1 and GD1a (trace to 12.6%), were isolated from these cells. The relative amount of GM3 in cALL cells was found to be about double that in normal lymphocytes (65.7% vs. 37.7%), but lower than in chronic lymphocytic leukaemia (CLL) cells (65.7% vs. 81.5%). The cALL cells contained trace amounts of the ganglioside GD3, a compound present in CLL cells (5.6%) but absent in normal lymphocytes.
Adolescent↗
Gangliosides in human chronic lymphocytic leukaemia.
Gangliosides were analysed by elaborated overpressured thin-layer chromatography (OPTLC) in 6 cell samples from 5 patients with chronic lymphocytic leukaemia (CLL) of B-cell origin, and 4 individual lymphocyte preparations from normal blood donors. The principal difference in the ganglioside profile between these two counterparts appears to be the presence of GD3 and the predominance of the less polar compounds (GM3, GM2, GM1) in CLL cells. Qualitatively, GD3 accounted for about 5.5% of the total CLL gangliosides, whereas it was not detectable in normal lymphocytes. Quantitatively, GM3 constituted more than 81% of the total CLL gangliosides, a proportion more than twice as high as that found in normal lymphocytes. Three other minor gangliosides were isolated from CLL cells; these were shown to be GM2 (trace amounts), GM1 (7.7%), and GD1 (4%). The expression of individual gangliosides varied greatly among the various CLL samples obtained from different patients, and even from the same patient, if examined at different times. No gangliosides were found in the supernatant collected from CLL cells subjected to a temperature shift (0 degrees C to 37 degrees C) or in the cell-free medium harvested from the CLL cells kept in overnight culture.
Aged↗
Appearance of covalently bound antigen in immune complexes formed during the activation of complement.
The effects of complement activation on the antigenic component of immune complexes have been studied, using 125I-BSA-rabbit anti-BSA-IgG complexes as models. Polyethylene glycol precipitates of 4 types of IC (those formed in native normal human serum, or NHS-containing EDTA, NHS-EDTA, and preformed soluble IC incubated in NHS or NHS-EDTA immediately after preparation) were analysed by sodium dodecyl sulphate-polyacrylamide slab gel electrophoresis. A characteristic difference in the distribution of 125I-BSA in the gel was observed between the NHS- and NHS-EDTA-treated samples. With the former type of IC, a significant part (16-23%) of the label was found in gel fractions of mol. wt. exceeding that of the antigen (80-300 kDa vs. 69 kDa), whereas with NHS-EDTA-treated IC only a minimal amount (4-5%) of the radioactivity was detected in these fractions. These findings indicate that complement activation results in the covalent binding of complement to the antigenic component of IC. The practical importance of these observations is discussed. In addition, a marked difference in precipitability was observed between IC formed in NHS and preformed IC incubated in NHS.
Antigen-Antibody Complex↗
Antibodies to primate retrovirus antigens in circulating immune complexes of patients with acute myeloid leukemia.
Circulating immune complexes were isolated from sera of 8 patients with acute myeloid leukemia (AML) in relapse, and 20 healthy blood donors. F(ab')2 fragments were prepared from the isolated complexes. Using a radioimmunoassay (RIA), these F(ab')2 fragments, the undigested complexes and the original sera were examined for the presence of antibodies against a panel of primate retrovirus antigens: gp70, p15 and p30 of gibbon ape leukemia virus (GaLV) and baboon endogenous virus (BaEV). F(ab')2 fragments derived from the immune complexes of all patients reacted with one or more of the antigens tested, whereas no antibody activity was found in the sera or undigested immune complexes of the same patients. By a competitive RIA, antigens related to GaLV and/or BaEV were found in the serum of 7 out of 8 patients. No markers of these retroviruses were detected in the F(ab')2 preparations, in immune complexes or in sera of any of the 20 control subjects. Our results indicate that a part of the circulating immune complexes in AML contain antigens related to primate retroviruses and specific antibodies to these antigens.
Adult↗
Precipitability and composition of HBsAg-anti-HBs immune complexes formed in the presence of complement. A model of circulating immune complex analysis.
Immune complexes (IC) of partially purified HBsAg and human anti-HBs were prepared at different antigen/antibody ratios in the presence of complement in normal human serum (NHS), and under conditions not allowing complement activation in buffers or in NHS containing 10 mM EDTA (NHS-EDTA). Commercial preparations of the radiolabelled antigen and antibody were used. IC formed in NHS were not significantly precipitated even after incubation for 24 h at 4 degrees C, whereas a typical precipitation curve was observed with complexes formed in the absence of complement. Thus, complement activation was found to markedly and permanently inhibit precipitability of HBsAg-anti-HBs immune complexes (HBsAg-IC). HBsAg-IC were precipitated from sera with 3.5% polyethylene glycol (PEG), boiled in sodium dodecyl sulphate (SDS)-urea buffer, and analysed by SDS-polyacrylamide slab gel electrophoresis (SDS-PAGE). With complexes formed in the presence of complement, about one-sixth of the antibody activity was found in high molecular weight fractions corresponding in size to IgG oligomers. By contrast, with complexes formed without complement, no significant amount of antibody was found in these fractions. With blotting technique and radiolabelled anti-human-C3 antibody, it was demonstrated that anti-HBs was covalently bound to C3b fragments in IC formed in the presence of complement and was in the high molecular weight fractions.
Animals↗
Hepatitis B surface antigen circulating immune complexes (HBsAg-CICs) in patients with bleeding disorders.
Approximately 90% of 67 multi-transfused patients with bleeding disorders were positive either for anti-HBs (85%) or HBsAg (45%). Using a polyethylene glycol trypsinization assay, we found anti-HbsAg-containing specific circulating immune complexes (HBsAg-CICs) in 3 of the 57 HBsAg-negative haemophiliacs possessing anti-HBs. The occurrence of HBsAg-CICs may be a regular event in the conversion phase of HBs infection. Circulating immune complexes as detected by the anticomplementary assay were found in 32 of the 67 (48%) patients.
Alanine Transaminase↗
Hepatitis B surface antigen circulating immune complexes (HBsAg-CICs) in patients with hepatitis B and asymptomatic HBsAg carriers.
The PEG-trypsinization assay detected HBsAg-CICs in 31 out of 44 (70%) patients with acute hepatitis B, in five out of 107 (5%) asymptomatic HBsAg carriers and, in addition, in both patients with HBsAg-positive chronic liver disease. A close correlation between the levels of HBsAg-CICs and disease activity was observed. The clinical course, parameters of liver function tests and outcome of the disease in patients without HBsAg-CICs (group A) and in patients with transient HBsAg-CICs (group B) were essentially similar. In contrast, patients with persistent HBsAg-CICs (group C) had a poor prognosis, particularly those who received corticosteroids. The method appeared to be a valuable tool in monitoring disease activity and prognosis, and in evaluating the efficacy of corticosteroid treatment. The role of HBsAg-CICs in the pathogenesis of liver damage and clearance of circulating HBsAg is discussed.
Acute Disease↗
Detection and quantitation of hepatitis-B surface antigen immune complexes (HBsAg-ICs) by an antigen-specific method. I. Detection and quantitation of in vitro prepared HBsAg-ICs.
An antigen-specific method has been developed for direct detection and quantitation of HBsAg-ICs. The method involves (1) precipitation of HBsAg-ICs with 3.5% PEG; (2) dissociation of the PEG precipitated ICs by treatment with NaSCN, NaI, KBr, low or high pH buffers, trypsin or papain; and (3) detection and titration of HBsAg and/or anti-HBs liberated from ICs. Treatment with 2 M and 3 M NaSCN, papain or trypsin liberates HBsAg, while following treatment with 3 M and NaI free anti-HBs is detectable. Trypsin digestion (2 mg/ml, 30 min at 37 degrees C) proved to be most effective for disrupting HBsAg-ICs formed at equivalence as well as in excess of antigen or antibody. After trypsin digestion of the sample RPHA, RIA and ELISA may be used as a third step. Th
Antibodies↗
Detection and quantitation of hepatitis B surface antigen immune complexes (HBsAg-ICs) by an antigen-specific method. II. Circulating immune complexes (CICs) in patients with hepatitis B and asymptomatic HBsAg carriers.
Using the PEG-trypsinisation assay, HBsAg-CICs were detected in 70% of patients with acute hepatitis B, in 5% of the asymptomatic HBsAg carriers and, in addition, in each of the 2 cases of chronic hepatitis B virus infection. In serial examinations, the complexed HBsAg levels in 77% of patients with acute hepatitis B decreased progressively in parallel with the free HBsAg levels, and persisted in the remaining 23%. In 19% of patients positive for HBsAg-CICs, the complexed HBsAg levels were higher than those of free HBsAg. No correlation was observed between results of PEG-trypsinisation and an anticomplementary assay. Artificial HBsAg-ICs in antigen excess were found to be poorly anticomplementary. C3 concentrations were normal or elevated in the majority (88%) of sera positive for HBsAg-CICs. These findings suggest that HBsAg-CICs in antigen excess are unlikely to be complement-activating. The method is useful for clinical investigation and for routine examination for HBsAg-CICs.
Adolescent↗