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)

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

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

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

A subset of normal peripheral B lymphocytes expresses a T surface antigen recognized by monoclonal CD5. They form rosettes with mouse erythrocytes (MRBC). Other studies suggest that these B cells may have regulatory and helper properties. An expanded subset of lymphocytes forming MRBC was demonstrated in the peripheral blood of 31 Systemic Lupus Erythematosus (SLE) patients (14.4 +/- 2.8%) compared with normal controls (4.3 +/- 1.4%) and patients with tuberculosis (6.4 +/- 1.7%). Increased MRBC values correlated with disease severity. Investigation of cell surface antigen expression was attempted with enriched sedimented fractions using several monoclonal antibodies and immunofluorescent staining. Complete inhibition of MRBC formation was obtained with monoclonal antibodies against CD5, CD3 and CD8 while partial inhibition was observed with anti-Ia and no activity with CD4 and CD10 antibodies. Indirect evidence supports the concept that antilymphocyte antibodies cause T and B cell depletion and dysfunction. Sera from 12 patients with SLE and 28 with leprosy (LL) were analyzed for antibodies to lymphocytes in the microcytotoxicity assay: 87% of SLE and 57% of LL were positive. Lymphocytotoxic activity towards each cell type of a panel with 98 different HLA antigens was essentially the same and most sera were not specific for either T or B cells. Lymphocytotoxic sera from SLE and LL contained antibodies which inhibited MRBC formation.
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PMID:[Lymphocyte imbalance in autoimmunity]. 264 Apr 77

B lymphocytes bearing the Leu-1 cell-surface antigen (Leu-1+), the human equivalent of mouse Ly-1+ B lymphocytes, have been detected in human peripheral blood, but there is little information on their frequency and properties. Analysis by fluorescence-activated cell sorter and double immunofluorescence showed that Leu-1+ B cells are consistently present in the peripheral blood and spleens of healthy subjects and constitute 17.0 +/- 5.0% (mean value +/- standard deviation) and 17.3 +/- 3.9%, respectively, of total B cells. When purified Leu-1+ and Leu-1- B lymphocytes were transformed into immunoglobulin-secreting cells by infection with Epstein-Barr virus and the culture fluids were tested for reactivity with self-antigens, at least two important autoantibodies, antibody to the Fc fragment of human immunoglobulin G (rheumatoid factor) and antibody to single-stranded DNA, were found to be made exclusively by Leu-1+ B cells. It is concluded that the Leu-1+ lymphocytes represent a major subset of the normal human B cell repertoire and include the B cells capable of making autoantibodies similar to those found in systemic lupus erythematosus and rheumatoid arthritis.
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PMID:Human lymphocytes making rheumatoid factor and antibody to ssDNA belong to Leu-1+ B-cell subset. 310 56

Since the immune response in fetuses of mothers with systemic lupus erythematosus (SLE) is unknown, we investigated sera from six mothers and their paired offspring by enzyme-linked immunosorbent assay (ELISA) for the presence of a common anti-DNA idiotype (16/6 Id) and, as control, for the presence of an unrelated public idiotype of antibody to hepatitis B surface antigen (HBsAg). In addition, maternal as well as fetal sera were evaluated for the presence of antibodies to ssDNA, dsDNA, poly(I), poly (dT), RNA, cardiolipin, total histones and the presence of lupus anticoagulant. Clinically active SLE mothers showed in general increased IgG and, to a lesser extent, IgM autoantibody activity. Circulating lupus anticoagulant was detectable in clinically active mothers only. All offspring of clinically active SLE mothers showed increased IgG autoantibodies to a variety of antigens, while IgM antibodies were detected in only one fetus. In contrast, fetuses of clinically inactive mothers showed only minor IgG activity. Common anti-DNA-idiotype (16/6 Id) activity also correlated with disease activity in both maternal and fetal compartments. One clinically active mother was 16/6-negative; her offspring was, however, positive, indicating de novo production of the idiotype by the fetus. In contrast, a control anti-HBsAg idiotype was not detected in either maternal or fetal sera. It therefore appears that offspring of clinically active SLE mothers serologically reflect maternal disease activity. Furthermore, autoantibodies and common idiotype of autoantibodies can be found within the fetal compartment even in the absence of such antibodies in the maternal serum. Discrepancies between mothers and offspring in IgM-autoantibody levels and the presence of new idiotypes in fetuses are indicative of fetal de novo autoantibody production.
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PMID:A common anti-DNA idiotype and other autoantibodies in sera of offspring of mothers with systemic lupus erythematosus. 311 49

To evaluate the performance of a serological test for human immunodeficiency virus type 1 (HIV-1) infections based on the use of a recombinant envelope gene-derived protein as the antigen, we caused expression of a 1.4-kilobase fragment of HIV.DNA that codes for the complete gp41 transmembrane protein in an Escherichia coli expression vector and used Western blots (WB; immunoblots) prepared with recombinant material (pEX-41) to detect antibodies to HIV-1. This test detected all 339 sera which were positive by a combination of conventional serodiagnostic assays and produced no false-positive results with 311 negative samples. Also no false-positive results were obtained with 20 sera from systemic lupus erythematosus patients which had high titers of cross-reactive autoantibodies. In six cases, the pEX-41 WB proved to be more sensitive than individual assays applied on their own, and in five cases it was even more sensitive than a combination of conventional assays. We tested 221 sera in both our pEX-41 WB and a commercially available recombinant enzyme immunoassay (EIA [Abbott]). The results were identical in 188 cases. A total of 27 sera containing antibodies to gp41 as demonstrated in the pEX-41 WB, as well as the Abbott recombinant EIA, had no antibodies to the recombinant core antigen as measured in the Abbott EIA. However, 25 of these sera did stain the 24-kilodalton band on a WB with purified virus. Six sera that were positive in all of the conventional confirmatory assays and reacted strongly with the pEX-41 WB did not recognize the surface antigen used in the Abbott recombinant EIA. We conclude that the use of WB prepared with recombinant-derived p41 offers a very sensitive and specific method to detect antibodies to HIV.
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PMID:Comparison of Western blot (immunoblot) based on recombinant-derived p41 with conventional tests for serodiagnosis of human immunodeficiency virus infections. 327 88

The clinical data and renal pathologic information from three patients with systemic lupus erythematosus (SLE), active glomerular disease, and hepatitis B virus (HBV) antigenemia are presented. All three patients fulfilled the American Rheumatism Association criteria for the diagnosis of SLE. However, the renal pathologic results excluded the diagnosis of lupus nephritis. The common findings shared by these patients included the following: presence of hepatitis B surface antigen (HBsAg) in both serum and glomeruli and of glomerular hepatitis B core antigen (HBcAg), and the absence of polyclonal immunoglobulins, C1q and C4, deposition in renal tissue. These common features and the renal pathologic results indicated that the glomerulopathy was associated with HBV antigenemia. The cases described here may represent a subset of patients with SLE in whom expression of lupus nephritis was altered by the concomitant HBV-related glomerulonephritis.
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PMID:Hepatitis B virus-related glomerulopathy in patients with systemic lupus erythematosus. 331 Jun 6

One hundred patients with systemic lupus erythematosus (SLE) were investigated for serological markers of hepatitis B virus (HBV) and had liver function evaluated. One patient had hepatitis B surface antigen and 25 had antibodies to HBsAg which is not significantly different from normal blood donor controls. Minor liver function abnormalities were found in 35 patients and there was no difference between those with and without anti-HBs. A single patient without HBV markers had more severe liver enzyme elevation. Our data do not show a relationship between SLE and HBV and support the contention that liver diseases in lupus is mild.
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PMID:Hepatitis B virus infection and liver function in patients with systemic lupus erythematosus. 356 91


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