Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The C1q precipitin test was performed in serum samples from five groups of patients: (1) 20 patients with acomplementemic systemic lupus erythematosus glomerulonephritis (SLE), (2) 2 patients with serum sickness due to the administration of horse serum, (3) 2 patients with serum sickness preceding hepatitis B, (4) 50 patients with chronic urticaria, and (5) 30 normal controls. Positive C1q precipitin tests were found in all patients with SLE and the four cases of serum sickness. Positive tests correlated with depressed serum complement (C3 and C4) levels and were found only in the early phase of serum sickness. Urticaria patients uniformly had negative C1q precipitin tests and normal serum complement levels.
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PMID:Studies of urticaria and acute serum sickness with the C1q precipitin test. 13 55

Polymorphonuclear leucocytes (PMN) from patients with systemic lupus erythematosus (SLE) were isolated from defibrinated and heparinized blood. In addition, PMN from a healthy donor were incubated with sera from SLE patients and with sera containing artificially prepared immune complexes of hepatitis B surface antigen (HBsAg) and human anti-HBsAg immunoglobulin (anti-HBs) with well defined variations of the antigen/antibody ratio. To one group of blood samples, 5 mM monoiodine acetic acid (MIAA) was added to block in vitro phagocytosis. The Pmn were examined for the presence of IgG, IgM, and HBsAg by the immunofluorescence technique. PMN from defibrinated blood of SLE patients showed in up to 80% immunoglobulin (Ig)-inclusions. However, addition of 5 mM MIAA reduced the number of Ig-containing PMN to at most 40%, which levels were equal to numbers found in specimens from heparinized blood. Addition of 5 mM MIAA to heparinized blood did not reduce the number of PMN with Ig inclusions. Normal donor PMN isolated from defibrinated, heparinized, and EDT blood showed equal amounts of Ig inclusions after incubation with SLE sera, but none when MIAA had been added. In PMN incubated with HBsAg-anti HBs immune complexes with an antigen antibody ratio between 5 and 0-2, both HBsAg and IgG could be detected. It is concluded that Ig inclusions in PMN from heparinized blood from SLE patients are due to in vivo phagocytosis, presumably of circulating immune complexes. In vitro phagocytosis of Ig from SLE sera by normal donor PMN also suggests the presence of immune complexes. Dependent on the antigen-antibody ratio, artificial HBsAg/anti-HBs immune complexes can be detected by in vitro phagocytosis by PM.
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PMID:Immune complex detection by immunofluorescence on polymorphonuclear leucocytes. 32 68

Thirty of 85 children with membranous glomerulonephritis (MGN) had associated extraglomerular disorders. The relation of these associations to membranous glomerulonephritis (MGN) is discussed. The causal relationship of acute hepatitis (5 cases), persistent hepatitis B antigenemia (6 cases), systemic lupus erythematosus (2 cases) and syphilis (1 case) may be ascertained; in similar conditions a definite antigen (Ag) has been found in MGN deposits. The association with SS or SA hemoglobinopathy (3 cases) ans with a preceding streptococcal infection (4 cases) raises the possible responsibility of renal tubular epithelium (RTE) Ag and of a streptococcal Ag. D-penicillamine therapy (1 case) is a well-known cause of MGN although the acting Ag remains unknown. Four children had serum sickness-like symptoms, two had hematologic disorders and two had proximal tubular dysfunction, one of them with proven anti-tubular and anti-alveolar basement membrane antibodies. A decrease in plasma C4, Clq, and factor B with normal C3 was frequently observed. The multiple Ag previously described as causative of MGN are recalled. The prevalent incidence of HBsAg is stressed, and the necessity for further investigations in patients with MGN in order to find an underlying disease is emphasized.
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PMID:Membranous glomerulonephritis with extra-renal disorders in children. 44 58

The search for circulating immune complexes by precipitation tests using polyethylene glycol (PEG) was performed on a series of normal and pathological sera. Various factors affecting PEG precipitation were studied. Immunoglobulins and complement factors percipitated by PEG (3.5%) were quantified and their significance was discussed in relation to serum levels. The PEG test was compared to labeled C1q binding test with a fairly good correlation. The direct evaluation of the amount of C4 precipitated with IgG by 3% PEG (C4 test) provided a simpler routine assay than the C1q binding test for detecting complement-fixing immune complexes. The direct PEG test and the C4 tests gave positive results in patients with diseases generally presumed to be associated with immune complexes including systemic lupus erythematosus, acute glomerulonephritis, bacterial sub-acute endocarditis and chronic acitve hepatitis. The demonstration of HBs antigen and antibody after acid dissociation of PEG precipitates from hepatitis B seronegative sera illustrated the fact that PEG does precipitate and thus concentrates circulating immune complexes.
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PMID:Detection of circulating immune complexes in human sera by simplified assays with polyethylene glycol. 88 55

Sera from 22 patients with systemic lupus erythematosus (SLE) were examined for the presence of hepatitis B antigen (HBsAG) by a complement fixation (CF) test, by an immunoelectrophoretic method (counterelectrophoresis-CEP), and by radioimmunoassay (RIA). The sera from 8 patients gave positive results using CF. However, the same sera and sera from 28 additional SLE patients, when tested with CEP and RIA, were not shown to contain HBsAG.
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PMID:Hepatitis B antigen and systemic lupus erythematosus. False positive complement fixation due to anti-antibodies. 108 49

Abnormal processing of immune complexes (IC) may be important in the pathogenesis of systemic lupus erythematosus (SLE). The clearance of large soluble IC (comprising hepatitis B surface antigen (HBsAg)/anti-HBsAg) radiolabeled with 123I was examined in 12 normal subjects and 10 patients with SLE. IC localization was analyzed by static and dynamic gamma-scintigraphy. Initial IC clearance from blood was more rapid in patients (median t1/2 = 2.15 min) than normals (median t1/2 = 5.15 min) due to more rapid uptake in the liver. However, in the SLE group, up to 12% of complexes were released from the liver after 30-50 min. Splenic uptake of immune complexes was reduced in the patients and there was reduced ability to retain IC in this organ. Plasma complement levels and erythrocyte complement receptor type 1 numbers were reduced in the patients, resulting in defective opsonization of IC and reduced red cell binding in vivo. These observations support the hypothesis that IC handling is abnormal in SLE.
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PMID:Immune complex processing in patients with systemic lupus erythematosus. In vivo imaging and clearance studies. 143 Feb 31

C3b-coated immune complexes adhere to the complement receptor 1 (CR1, CD35) on human erythrocytes. This multi-valent binding might be favoured by the known clustering of CR1 and by the multiple C3b-binding sites on each CR1. The size of the CR1 clusters correlates directly with the number of CR1/erythrocytes, and the different structural CR1 alleles bear between two and five C3b-binding sites. Using radiolabelled hepatitis B surface antigen-antibody complexes, we investigated whether CR1 numbers and structural alleles modulate the ability of erythrocytes to bind immune complexes, and assessed if any reorganization of immune complexes takes place at the erythrocyte surface after the initial binding reaction. The binding efficiency (immune complexes/CR1) correlated with CR1 number as determined by the maximal binding at 4 degrees C, the kinetics of binding at 37 degrees C, and the binding in the presence of excess immune complexes and of immune complexes of small size. Binding efficiencies were similar for erythrocytes with low CR1 from normal subjects and patients with AIDS or SLE. A monoclonal antibody blocking the C3b-binding sites (3D9) of CR1 interfered with binding efficiency at a lower concentration on cells bearing low CR1 numbers, suggesting that CR1 clustering is essential. The larger alleles of CR1 (DD and BB) were more efficient than AA alleles. The distribution of immune complexes, visualized by immunofluorescence, was heterogeneous on erythrocytes: about two out of three cells bore between one and 12 immune complexes. No visible immune complex reorganization took place after initial binding, as prefixed erythrocytes displayed the same immune complex distribution and number/erythrocytes as unfixed erythrocytes. The contribution of CR1 alleles in immune complex binding efficiency was confirmed by morphological analysis. These results demonstrate that immune adherence efficiency is the resultant of the CR1 clustering, as well as the particular alleles carried by erythrocytes. Moreover, there is little or no immune complexes surface reorganization after the initial binding reaction.
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PMID:Immune complex binding efficiency of erythrocyte complement receptor 1 (CR1). 182 50

Complement levels and complement receptor 1 (CR1) on erythrocytes (E) are reduced in systemic lupus erythematosus (SLE). To see whether these abnormalities are responsible for defective transport and elimination of immune complexes (IC) from the circulation, patients with active SLE (14) and normal volunteers (14) were injected with preformed IC (hepatitis B surface Ag/Ab). Two minutes after injection only 25.9 +/- 19.1% (mean +/- 1 s.d.) of the circulating IC were bound to E in the SLE patients as compared to 63 +/- 3.7% in the normal subjects (P = 0.0001). For SLE patients, the reduced immune adherence was best explained by a combination of complement depletion and low CR1 binding capacity (tau = 0.80, P = 0.0001). The disappearance of IC as estimated from the area under the elimination curve was faster in SLE than in controls (P = 0.02), and correlated with CR1 (tau = 0.54, P = 0.0001) and immune adherence observed in vivo (tau = 0.33, P = 0.013). Finally, immune adherence was absent and IC disappeared very rapidly in a patient with C2 deficiency and an SLE-like disease. These observations suggest that in SLE the defective immune adherence reaction might be responsible for the accelerated disappearance of IC from the circulation.
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PMID:Immune adherence and clearance of hepatitis B surface Ag/Ab complexes is abnormal in patients with systemic lupus erythematosus (SLE). 189 16

Among 30 consecutive patients diagnosed with primary biliary cirrhosis (PBC) in Taiwan, 27 were females and the median age of symptom onset was 54.5 years. Most had similar clinical manifestations to those reported in the Western countries, but ascites and oesophageal varices as commonly found at the late stages of cirrhosis of liver were noted in nine patients (30%) and 13 patients (43%) respectively. Only one patient was asymptomatic. Hyperbilirubinaemia was noted in 21 patients (70%) and hypoalbuminaemia in 8 patients (27%). All patients had elevated serum alkaline phosphatase and alanine aminotransferase and 28 (93%) had antimitochondrial antibodies. Ten out of 21 patients (48%) were positive in antinuclear antibodies, of which most were of speckled type. Sixteen out of 18 patients (89%) had elevated serum IgM levels. Interestingly, only one of 26 patients (3.8%) was positive for hepatitis B surface antigen, in contrast to its high prevalence (15%) in the Taiwan population. Special associated diseases, including systemic lupus erythematosus, scleroderma, malignant lymphoma and hepatocellular carcinoma, were each noted in one patient respectively. Eight patients had a history of gallstones before the diagnosis of PBC. The mean follow-up period was 23.6 +/- 19.8 months, and nine patients died during that period. In conclusion, the clinical manifestations of PBC in Taiwan are similar to those in Western countries, but most of our cases were at later stages.
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PMID:Primary biliary cirrhosis in Taiwan. 212 28


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