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)

The human C3b receptor (CR1) is a polymorphic glycoprotein which functions regulating the complement system by inhibiting the activation of C3 and C5, through its effect on their convertases, and serving as cofactor for factor I in mediating the degradation of C3b to its inactive fragment C3bi and further to C3d-g. The latter are then ligands for their respective receptors on leukocytes, CR3 and CR2. Additionally, CR1 on erythrocytes endows these cells with the capacity to deliver immune complexes (IC) to the reticuloendothelial system, resulting in their clearance from the circulation. On phagocytes, this receptor participates in the process of endocytosis of foreign particles. There is a wide inherited variation of CR1 expression on erythrocytes (CR1/E) of different individuals. Patients with diseases which feature elevated levels of IC, such as systemic lupus erythematosus, leprosy, and AIDS, have a marked decrease of CR1/E, which may result in an altered clearance. This reduction appears to be related to disease activity, and the most probable site for CR1/E loss is during the transfer of IC to macrophages. Healthy neutrophils increase tenfold their expression of CR1 in response to the effect of chemoattractant peptides. Neutrophils from patients with AIDS display an altered response to stimulation. This defect may be of relevance in the process of endocytosis.
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PMID:The human C3b receptor: function and role in human diseases. 214 Oct 47

We describe a case of systemic lupus erythematosus (SLE) with nephrotic syndrome who suffered from myocardial infarction and cerebral infarction associated with hyperLp(a)aemia. The proband was an 18-year-old Japanese male who was found to have hypercholesterolemia and hyperLp(a)aemia, with a serum total cholesterol level of 361 mg/dl and a serum Lp(a) level of 197 mg/dl. His father and mother showed higher Lp(a)levels (26 and 56 mg/dl, respectively) than those in normals (18 +/- 0.6 mg/dl, mean +/- SE). Lp(a)glycoprotein phenotypes were examined. The proband had the phenotype S2/4, which is associated with high Lp(a) concentration. His parents had the phenotype S3/4 and S2/4. No cardiovascular diseases were noted in other members of his family. After treatment with CS-514, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase. Lp(a) levels decreased from 197 to 121 mg/dl, but still remained abnormally high. LDL apheresis using a Liposorber system was attempted in this patient. Total and LDL cholesterol levels decreased by 57 and 62%, respectively. Lp(a) levels decreased by 68%. These results suggest that LDL apheresis may be an alternative therapy in drug resistant hyperLp(a)aemia.
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PMID:A case of hyperLp(a)aemia, associated with systemic lupus erythematosus, suffering from myocardial infarction and cerebral infarction. 214 57

1. Binding to and destruction of basement membrane (BM) are necessary steps for cancer cells to extravasate and metastasize. Serum levels of released BM components may correlate with the staging of human cancers or with inflammatory disorders. Furthermore, released material may also induce autoantibodies. Since laminin, an 800-kDa glycoprotein, is present in the extracellular matrix, serum laminin levels may be markers of BM injury. 2. A two-site enzyme immunoassay and a radioimmunoassay were developed to test sera from patients with breast cancer or systemic lupus erythematosus (SLE). 3. A significant difference in laminin concentrations was demonstrated between early (T0-T2) and advanced (T3-T4) tumors (P = 0.001). However, specimens from SLE patients did not differ in laminin concentration from normal individuals and no correlation was observed between laminin levels and anti-laminin auto-antibody titers. 4. These results suggest that serum laminin levels are useful markers of BM damage and could be of prognostic value in cancer.
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PMID:Two-site immunoassays for the measurement of serum laminin: correlation with breast cancer staging and presence of auto-antibodies. 220 42

A variety of tubular marker proteins, as compared to healthy controls, are excreted at an increased rate in the urine of patients with renal damage. Beside cytoplasmic glutathione-S-transferase and lysosomal beta-N-acetyl-glucosaminidase (beta-NAG) the majority of kidney-related urine proteins derives from membrane surface components of the most vulnerable proximal tubule epithelia, among them ala-(leu-gly)-aminopeptidase, gamma-glutamyl transpeptidase (GGT), the tubular portion of angiotensinase A, the major brush border glycoprotein 'SGP-240' and adenosine-deaminase-binding protein. Urinary tissue proteins, e.g. brush border (BB) microvilli, are immunologically identical with those antigens prepared from cell membranes of the human kidney itself. BB antigens are shed into the urine of patients with glomerulonephritis, interstitial nephritis, systemic diseases, e.g. systemic lupus erythematosus (SLE), diabetes mellitus and multiple myeloma, arterial hypertension, infectious diseases (malaria, AIDS) and after operations, renal grafting and administration of X-ray contrast media, aminoglycosides or certain cytostatics (cis-platinum). Tissue proteinuria of tubular proteins is determined by enzyme-kinetic or quantitative immunological assays applying either poly- or monoclonal antikidney antibodies. Clinical, ultrastructural and histochemical studies support the idea that both 'soluble' and high-molecular-weight membrane particles (vacuolar blebs, greater than 10(6) dalton) as well as microfilamental components of the epithelial cytoskeleton contribute to tubular 'histuria' which appears as a sensitive parameter in monitoring tubular damage under clinical conditions at a very early phase.
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PMID:Urinary proteins of tubular origin: basic immunochemical and clinical aspects. 225 76

Serum alpha 2HS-glycoprotein (A2HSG) concentrations of 63 patients with systemic lupus erythematosus (SLE) were determined, and found to be significantly low compared to those of 59 healthy blood donors. The diminution of serum A2HSG concentration was proportional to the degree of activity of SLE, and was not influenced by secondary infections. There was a statistically significant positive correlation between serum A2HSG and the C3 complement component levels. A negative correlation between serum A2HSG and IgG, IgA concentration and anti-DNA activity was observed. Serum A2HSG was significantly low in cases of positive for the following laboratory parameters: anti-nuclear antibodies, circulating immune complexes and LE cell phenomenon. We found no correlation between serum IgM concentration, cryoglobulins, latex agglutination and serum A2HSG levels. The unusually good negative correlation between A2HSG pathogenetical role of this glycoprotein in SLE. The determination of A2HSG concentration may be of clinical importance in SLE.
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PMID:Correlations between serum alpha 2-HS-glycoprotein concentration and conventional laboratory parameters in systemic lupus erythematosus. 228 Sep 96

The antibody response to the structural proteins of rubella virus was studied in patients with multiple sclerosis (MS). Irrespective of the antibody titer to whole rubella virus, the relative proportion of the IgG response to the surface glycoprotein E1 was diminished, and that to the surface glycoprotein E2 was elevated in MS patients when compared to a matched control population of normal health individuals or a group of patients with systemic lupus erythematosus and other collagen vascular diseases. No difference was observed in the response to the core protein of rubella virus on comparing the MS and normal control groups. This divergence in the relative antibody response to the viral surface proteins suggests that the vigorous antibody response to rubella virus reported in MS is not simply an expression of a nonspecific polyvalent B-cell response.
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PMID:Antibody response to rubella virus structural proteins in multiple sclerosis. 236 Jul 94

In vivo therapy with monoclonal antibody (mAb) GK1.5, which recognizes a glycoprotein antigen designated L3T4 on murine helper T lymphocytes, either prevented or suppressed the development of murine lupus, autoimmune encephalomyelitis, and collagen arthritis. The L3T4 antigen in the mouse is analogous to the human Leu-3/T4 antigen expressed on helper T lymphocytes, because they both participate in the T cell response to class II major histocompatibility complex (MHC) antigens. Class II MHC genes and I-A antigens mediate murine experimental autoimmune myasthenia gravis (EAMG) induced by acetylcholine receptor (AChR) autoimmunity. We studied the efficacy of mAb GK1.5 as an immunotherapeutic agent for murine EAMG. Therapy with mAb GK1.5 not only suppressed established autoimmunity to AChR but also prevented loss of muscle AChR in mice with EAMG. Moreover, permanent remission of clinical muscle weakness was induced if mAb GK1.5 therapy was initiated after the onset of clinical disease. Because the function of the Leu-3/T4 determinant on human helper T lymphocytes is analogous to the murine L3T4 determinant, use of antibody to the Leu-3/T4 determinant as an immunotherapeutic agent may provide a way to control the progression of human MG.
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PMID:Immunotherapy for myasthenia gravis: a murine model. 241 35

Several investigators have suggested that gastrointestinal inflammation has a role in the pathogenesis of ankylosing spondylitis. To test this hypothesis markers of gastrointestinal immunostimulation, as manifested by serum IgA concentrations, were compared with serum markers of inflammation, as manifested by acute phase proteins. Serum samples from 45 unrelated Caucasian patients with ankylosing spondylitis (AS) were tested for correlation of serum IgA and six acute phase proteins: C reactive protein (CRP), alpha 1-antitrypsin, alpha 1-antichymotrypsin, caeruloplasmin, alpha 1-acid glycoprotein (AGP), and haptoglobin. Serum IgA was shown to be significantly positively correlated with four of these six acute phase proteins: CRP (r = 0.58, p less than 0.001), alpha 1-antitrypsin (r = 0.29, p less than 0.05), AGP (r = 0.61, p less than 0.01), and haptoglobin (r = 0.58, p less than 0.001), suggesting that gastrointestinal immunostimulation does have a role in the pathogenesis of inflammation in AS. In addition, the microheterogeneity of the pattern of glycosylation of AGP, expressed as reactivity coefficients, was examined. The AGP reactivity coefficient has been shown to increase in infection, remain the same in systemic lupus erythematosus, and decrease in rheumatoid arthritis. It was found that the AGP reactivity coefficient was significantly decreased in patients with AS as compared with healthy controls (p less than 0.006). As recent studies have indicated that patterns of glycosylation reflect intrahepatocellular biosynthetic processes induced by cytokines our data suggest that cytokine-hepatocellular mechanisms in AS may be similar to those occurring in rheumatoid arthritis, but different from those in systemic lupus erythematosus or infection.
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PMID:Serum IgA, acute phase proteins, and glycosylation of alpha 1-acid glycoprotein in ankylosing spondylitis. 246 28

One of the mediators responsible for the induction of the production of acute phase proteins by hepatocytes is interleukin-6 (IL-6), formally known as hybridoma growth factor (HGF). In a prospective study the biological significance of IL-6, but also the relationship with the acute phase response (C-reactive protein [CRP], alpha 1-antitrypsin and alpha 1-acid glycoprotein) during flare-ups in 12 systemic lupus erythematosus (SLE) patients was investigated. Only 2 SLE patients showed sustained elevated IL-6 levels, and in one of these patients a clear correlation was found between the increases in IL-6 and the acute phase response. In the other SLE patients hardly any response or change in the levels of IL-6, CRP, and/or alpha 1-antitrypsin was found. In contrast to the profiles of alpha 1-acid glycoprotein, in seven of the SLE patients a significant increase in the serum levels took place in the period preceding the exacerbation. This difference between the three acute phase proteins suggests that the regulatory mechanisms are different. Our results are in agreement with the findings that IL-6 might be responsible for the CRP response.
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PMID:Interleukin-6 (IL-6) and acute phase proteins in the disease course of patients with systemic lupus erythematosus. 247 Dec 49

Affinity electrophoresis, with concanavalin A and Lens culinaris agglutinin as ligands, was applied to study the microheterogeneity of serum proteins, with special emphasis on alpha 1-fetoprotein and alpha 1-acid glycoprotein, two proteins of potential clinical value. A total of 602 samples of serum from patients with various neoplastic and inflammatory conditions were evaluated. Affinity electrophoresis provided useful information for differential diagnosis of cancers of various origins including hepatomas, metastatic liver cancers and yolk sac tumors. The method also proved indispensable for the detection of intercurrent infection in patients with rheumatoid arthritis, systemic lupus erythematosus and scaled burns.
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PMID:Affinity electrophoresis for diagnosis of cancer and inflammatory conditions. 247 61


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