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)

Clinical findings and structural alterations in the kidneys of 6 patients with sarcoidosis and an associated glomerulonephritis are described. Five of the 6 patients manifested the nephrotic syndrome during some phase of their illness. Additional clinical evidence of renal disease included persistent microscopic hematuria (5 patients), hypertension (4 patients) and progressive renal failure (3 patients). Glomerular pathology varied and included proliferative glomerulonephritis (3 patients), membranous glomerulonephritis (1 patient), and chronic glomerulonephritis (2 patients). In 2 patients sequential examination of the kidney was possible, with renal biopsies preceding autopsy examination by 3 and 6 years, respectively. Glomerular pathology had progressed in severity in each case. Immunofluorescent studies in 2 patients revealed patterns of glomerular antibody localization consistent with immune complex disease. Electron microscopic studies of 1 revealed membranous changes characterized by electron-dense subepithelial and intramembranous deposits. Totally unexpected were virus-like intraendothelial structures in the glomeruli identical to those previously reported in systemic lupus erythematosus. Since current evidence suggests that the pathogenesis of both membranous and proliferative types of glomerulonephritis is immunologic, it should not be surprising that sarcoidosis, a disease which quite possibly results from an immune response to a disseminated antigen(s), should occasionally include glomerulonephritis as a part of its histologic expression.
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PMID:Glomerulonephritis associated with sarcoidosis. 455 25

A sensitive and reproducible procedure for the detection of soluble immune complexes in sera from patients with various immunopathological disorders is reported. Radiolabeled C1q is reacted with sera containing immune complexes. Separation of free from complex bound [(125)I]C1q is achieved by selective precipitation with polyethylene glycol (PEG). The method is based on both the large molecular size and the C1q-binding property characterizing immune complexes. The minimal amount of aggregated immunoglobulins thus detected is about 10 mug and that of soluble human IgG-anti-IgG complexes is about 3 mug of complexed antibody. Some immune complexes formed in large antigen excess (Ag(2)Ab) can still be detected by this radiolabeled C1q binding assay. The specificity of the radiolabeled C1q binding test was documented by the inability of antigen-F(ab')(2) antibody complexes to lead to a precipitation of [(125)I]C1q in PEG. In a second step, this radiolabeled C1q binding assay was applied to an experimental model of immune complex disease and was shown to be efficient for the detection of in vivo formed immune complexes.Finally, the technique could be applied to the study of sera from patients with systemic lupus erythematosus (SLE) or to carriers of the hepatitis B antigen (HB-Ag). Significantly increased [(125)I]-C1q binding values were observed in 52 sera from SLE patients when compared to values obtained with healthy blood donors (P<0.001). Particularly high values were seen in active disease, a finding which was confirmed by follow-up studies performed with four SLE patients. No increased [(125)I]C1q binding was seen in 18 healthy carriers of the HB-Ag; whereas, sera from carriers with hepatitis appear to precipitate increased [(125)I]C1q percentages: 7/24 cases with acute transient and 4/7 cases with chronic persistent hepatitis were found to increasingly bind [(125)I]C1q. The results were also used for a correlative study of [(125)I]C1q binding to IgG levels in the sera but increased [(125)I]C1q binding could not be attributed to high serum IgG levels which are likely to account for gammaglobulin aggregates. These examples suggest the utility of the radiolabeled C1q binding assay for the evaluation of immune complex diseases in human pathology.
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PMID:Circulating immune complexes in the serum in systemic lupus erythematosus and in carriers of hepatitis B antigen. Quantitation by binding to radiolabeled C1q. 484 46

Immune-complex-mediated injury is thought to play a role in diseases such as rheumatoid arthritis, systemic lupus erythematosus, serum sickness, various infectious diseases, and malignancies. With increased appreciation of the biological and pathological significance of circulating immune complexes has come efforts to develop appropriate techniques for identifying and measuring them. Common approaches exploit such phenomena as the attachment of complement components to antigen-antibody complexes, the presence of specialized receptors for immune complexes at the surface of cells, and the ability of rheumatoid factor to bind with immune complexes. This variety of assay systems for immune complexes has yielded abstruse results in numerous human pathological conditions. Unfortunately, these results seldom correlate with one another in a given disease. Thus, use of a panel of immune complex assays has been recommended. Indirect consequences of immune complex disease may still be appraised and evaluated with some confidence in clinical medicine: measurements of C3 and C4, cryoglobulins, serum viscosity, and turbidity of serum samples. Measurement of immune complexes may be useful in diagnosis, prognosis, and therapeutic monitoring, but it is the characterization of immune complexes that holds the greatest potential for better understanding of disease mechanisms.
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PMID:Immune complexes: characteristics, clinical correlations, and interpretive approaches in the clinical laboratory. 621 Apr 68

A percutaneous renal biopsy was performed on a 50-year-old female with rapidly progressive renal failure. The histologic specimen was characteristic of an immune complex disease, most likely systemic lupus erythematosus. Serologic tests were negative. 8 days after the biopsy, there was a spontaneous rupture of the kidney which necessitated nephrectomy. As no connection was found between the biopsy site and the rupture, it was concluded that the rupture was spontaneous in a patient with an immune complex disease.
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PMID:Spontaneous rupture of the kidney in a patient with acute autoimmune disease. 621 71

Changes in the permeability of the blood-brain barrier (BBB) and blood-cerebrospinal fluid (blood-CSF) barrier in rabbits were assessed by using a sensitive double isotope technique at different times after the induction of acute immune complex disease (AICD). Induction of AICD was done with a single large dose of bovine serum albumin, whereas controls received only saline. Animals were sacrificed 6, 9, 12, 15, and 18 days after induction. Extravasation of protein was measured by injecting rabbits i.v. with 131I-rabbit serum albumin (RSA) 24 hr before sacrifice. In order to correct for intravascular blood volume, 125I-RSA was injected 5 min before sacrifice. Extravascular blood equivalents (EVBE), a measure of barrier permeability, were elevated in the CSF of rabbits sacrificed on days 12 and 15. None of the brain regions from any of the animal groups showed any changes or significant differences from controls in EVBE values on these days. These results indicate that there was an increase in the permeability of the blood-CSF barrier to radiolabeled albumin but not in the BBB proper during the time that CSF IgG levels were elevated in AICD. The potential significance of these findings for the mechanisms mediating central nervous system involvement in systemic lupus erythematosus is discussed.
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PMID:Permeability of the blood cerebrospinal fluid barrier during acute immune complex disease. 622 64

It has recently been reported that many immunological abnormalities including the presence of TSH-receptor antibody (TRAb) were found in Graves' disease (GD). Circulating immune complexes (CIC) have also been detected in the serum of patients with GD as observed in systemic lupus erythematosus, which is thought to be a typical model of immune complex disease. The role of CIC in pathogenesis of hyperthyroidism, however, remains to be elucidated. Therefore, to clarify pathophysiological functions of CIC in GD, the levels of it in those patients were compared with their symptoms, those of TRAb, and lymphoblastogenesis (LBG) induced by phytohemagglutinin (PHA), concanavalin A (Con A), and pokeweed mitogen (PWM). The subjects were forty patients with GD without any medication, one hundred and nine patients with GD on medication with methimazole (MMI), and fifteen healthy volunteers. CIC was measured by three different methods; polyethyleneglycol precipitation method (PEG), Clq binding assay (Clq), and Protein A binding assay (PA). The normal range was estimated with the mean plus or minus two times the standard deviation of normal controls. In untreated GD, CIC determined by PEG, Clq and PA widely distributed from normal range to high levels. The positive rates of CIC determined by PEG, Clq, PA, and any one method of these three were 17.5%, 22.5%, 30.0% and 52.5%, respectively. LBG using incorporation of tritiated thymidine showed the decreases in PHA and Con A, and the increases in PWM in patients with GD. The positive rates of CIC determined by PEG and PA were significantly higher in patients without goiter or with small one than those with large one (p less than 0.05). CIC measured by all three of PEG, Clq and PA showed negative correlation with TRAb significantly (p less than 0.05, p less than 0.01, p less than 0.01, respectively). On the other hand, CIC measured by Clq showed significant negative correlation with serum thyroxine concentration (p less than 0.01). The levels of CIC, TRAb and PWM-induced LBG decreased following the tapering dose of MMI sufficient to keep patients in euthyroid state. In consequence, there were no longer any correlations between CIC and TRAb after thyroid function was normalized. These observations suggest that CIC's which have huge molecular weight or have ability to bind Fc receptor on K cell, macrophage, neutrophil, and other immune cells may be one of the factors to inhibit the goitrogenic action of TRAb, and that CIC's which have ability to activate the complement system may be one of the factors to inhibit the stimulation of secretion of thyroid hormone by TRAb.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The role of circulating immune complexes in the pathogenesis of Graves' disease]. 632 60

C1q-precipitins (C1q-p) are comprised of 7S IgG with C1q-binding activity found in sera of patients with hypocomplementemic vasculitis urticaria syndrome ( HVUS ) and systemic lupus erythematosis (SLE). We have utilized C1q-coated polystyrene beads to selectively isolate C1q-p and to establish a sensitive and quantitative assay of C1q-p and immune complex activity. Purified C1q-p was comprised of polyclonal IgG which retained 7S sedimentation and solid phase C1q-binding activity at physiological ionic strength both in the presence and absence of normal human sera. No precipitation interaction was observed between C1q-p and fluid-phase C1q or C1 under the conditions tested. Purified C1q-p had no activity in the Raji cell immune complex activity. C1q-p activity also was observed in and purified from SLE serum; this activity was distinguishable from 7S immune complex activity detected by Raji cells which was also present in SLE serum. These studies indicate that C1q-p is a 7S IgG molecule found in HVUS as well as some SLE sera and has activity in C1q-binding but not in Raji cell-binding immune complex assays. These data also suggest that C1q-p is a monomeric, polyclonal IgG with preferential affinity for bound C1q. In addition to its potential role in immune complex disease, C1q-p may also provide an important tool for studying the interaction of immunoglobulin and C1q, and should contribute important information to understanding the pathobiology of immune complex disease.
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PMID:Assay, purification and further characterization of 7S C1q-precipitins (C1q-p) in hypocomplementemic vasculitis urticaria syndrome and systemic lupus erythematosus. 637 56

Radioimmune assay (RIA) was used to investigate the effect of fixatives on antigenicity of the hepatitis B surface antigen (HBsAg) and the effect of pronase on the elution of antibody (Ab) from the HBsAG-Ab complex. The effect of pronase on Ab elution was also tested on sections of kidney from a patient with the immune complex disease systemic lupus erythematosus (SLE). Immunoglobulin G (IgG) was located in pronase treated and untreated sections using the indirect immunoperoxidase technique. Glutaraldehyde was shown to be the fixative of choice for studies involving HbsAG. All fixatives were shown to have less effect on antigenicity at 4 degrees C than at room temperature. Osmium tetroxide reduced antigenicity to one-third, even at 4 degrees C. RIA and SLE kidney section studies showed that Ab was eluted from immune complexes by pronase. Pre-fixation of the antigen (Ag) by glutaraldehyde appears to have no effect on the final elution, although fixation after pronase treatment seemed to enhance the elution effects. The availability of an RIA kit with HBsAg- and AB-coated beads was of great assistance in evaluating reagents to be used in immunoperoxidase studies of HBsAg in immune complexes of patients with membranous nephropathy and Australia antigenaemia.
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PMID:The use of radioimmune assay in investigating reagents to be used in the immunocytochemical localization of hepatitis B surface antigen in immune complexes in the kidney of patients with membranous nephropathy and Australia antigenaemia. 641 96

Carr et al. (1978) and Rudin (1979) independently suggested tat systemic lupus erythematosus (SLE) might provide a model for schizophrenia since SLE is strongly associated with schizophreniform psychoses and exhibits only a covert CNS pathology revealed by immunofluorescent immune complex deposits in the choroid plexus. To carry the concept forward we here examine SLE employing the ideas developed in the preceding paper (Rudin, 1980) indicating that the choroid plexus is part of a second blood-brain barrier guarding the periventricular primary personality brain, the limbic system, and that the choroid plexus is also but one of a set of "transport organs" sharing common vulnerability to covert basal lamina immune complex pathology. In this context both SLE and schizophrenia are viewed as expressions of combined transport dysfunction syndromes, resulting from polygenic-induced sensitivity to exogenous peptides or viruses causing basal laminar immune complex disease, but exhibiting differing statistical expressions over the transport organ group due to difference in genes which elicit different transport organ sensitivities to different exogenous viruses or peptide antigens. Immune disease processes are briefly reviewed.
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PMID:The choroid plexus and system disease in mental illness. II. Systemic lupus erythematosus: a combined transport dysfunction model for schizophrenia. 645 11

Fc receptor-mediated mononuclear phagocyte system (MPS) clearance is impaired in systemic lupus erythematosus (SLE) and may contribute to the pathogenesis of the immune complex disease. To investigate the basis of MPS dysfunction, we have examined concurrent in vivo and in vitro Fc receptor function in 22 patients with SLE and 23 disease-free adults. Blood monocyte Fc receptor binding was increased rather than decreased as predicted by the saturation hypothesis of MPS blockade. Rosette formation of IgG-sensitized bovine erythrocytes (EA) with monocytes demonstrated increased Fc receptor-ligand binding in SLE (percent rosettes: 40 +/- 12 vs 27 +/- 8, p less than 0.001). Scatchard analysis of the binding of radiolabeled IgG oligomers to SLE monocytes indicated a mean receptor number 30% higher than control, although this did not reach statistical significance. Despite enhanced Fc receptor-ligand (EA) binding, Fc-mediated phagocytosis of EA was decreased in SLE (1.7 +/- 0.7 erythrocytes/monocytes/hour vs 2.6 +/- 1.0, p less than 0.004). This decrease in phagocytosis by blood monocytes from SLE patients was significantly greater than that attributable to the predominance in SLE of individuals with certain HLA B cell alloantigens and intrinsically lower phagocytic rates (p less than 0.05 for all groups). This decrease therefore represents a disease-acquired characteristic. Furthermore, the phagocytic rate of the four SLE patients with marked prolongation in MPS clearance was significantly lower than that of the eight patients with near normal clearance values (p less than 0.01). Saturation of Fc receptors by immune complexes does not explain impaired immune clearance in SLE. Our results indicate that despite increased binding of the EA ligand, Fc receptor-mediated phagocytosis is markedly impaired in SLE monocytes. This impairment cannot be explained on the basis of HLA-related differences in phagocytosis among lupus patients. The defect in phagocytosis of EA is most profound in those patients with the most significantly impaired MPS clearance. Thus, the dissociation of receptor-ligand binding and receptor-mediated internalization may contribute significantly to the in vivo clearance defect in SLE.
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PMID:Defective mononuclear phagocyte function in systemic lupus erythematosus: dissociation of Fc receptor-ligand binding and internalization. 648 Nov 62


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