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 effect of conditioned medium on the biosynthesis and glycosylation profile of acute phase proteins secreted by the human hepatoma cell line Hep G2 was studied. Conditioned medium was prepared from nonactivated [CM-LPS(-)] and ex vivo lipopolysaccharide activated [CM-LPS(+)] monocytes from eight patients with active rheumatoid arthritis (RA), five patients with active systemic lupus erythematosus (SLE), and seven healthy subjects. The biosynthesis of albumin, alpha 1-antichymotrypsin and alpha 1-proteinase inhibitor and the profile of glycosylation of proteinase inhibitor were analysed. CM-LPS(-) from patients with SLE had a similar effect to CM-LPS(-) from healthy subjects. In contrast, CM-LPS(-) from patients with RA had the same effect as CM-LPS(+) from healthy donors. A similar effect to that of CM-LPS(+) of healthy subjects was seen with CM-LPS(+) from patients with SLE and with CM-LPS(+) from patients with RA. The treatment of CM-LPS(+) with antibodies against interleukin 6 neutralised most of its ability to induce changes in the biosynthesis and glycosylation of acute phase proteins. Antibodies to interleukin 1 and tumour necrosis factor alpha had only a limited effect on the ability of CM-LPS(+) to induce changes of albumin and alpha 1-antichymotrypsin syntheses, whereas they had no effect on the biosynthesis and glycosylation of proteinase inhibitor. These results indicate that: (a) monocytes isolated from patients with active SLE and active RA have different capabilities of inducing alterations of acute phase proteins in vitro; (b) ex vivo activation of monocytes from patients with SLE leads to the full induction of its capabilities to change acute phase proteins, whereas the activation of monocytes from patients with RA has no additive effects; and (c) interleukin 6 seems to be a major cytokine involved in the regulation of the glycosylation pattern of acute phase proteins.
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PMID:Different capabilities of monocytes from patients with systemic lupus erythematosus and rheumatoid arthritis to induce glycosylation alterations of acute phase proteins in vitro. 137 63

alpha 1-antichymotrypsin, purified or in whole serum, exhibits microheterogeneous forms when studied by crossed immunoaffinoelectrophoresis with free concanavalin A (Con A) in the first dimension. alpha 1-antichymotrypsin purified from the serum of a single healthy donor was separated into three forms by affinity chromatography on a Con A-Sepharose 4B column: a Con A non-reactive form, a Con A weakly reactive form and a Con A reactive form. Some of their physico-chemical properties are compared. The complete primary structure of the glycans of each form was determined by high resolution 1H-NMR spectroscopy. The results indicated the presence of diantennary and triantennary type glycanic structures which occur frequently in serum glycoproteins. From deglycosylation experiments it is concluded that alpha 1-antichymotrypsin carries four oligosaccharide side chains. The Con A non-reactive form contains four triantennary glycans, the weakly reactive form contains three triantennary and one diantennary glycans and the Con A reactive form possesses on average one triantennary and three diantennary glycans. Significant variations in the relative ratios of the microheterogeneous forms were detected in various inflammatory syndromes. There is an increased proportion of Con A non-reactive form in patients developing a systemic disease (systemic lupus erythematosus, rheumatoid arthritis, temporal arteritis). In contrast, the proportion of Con A non-reactive form decreased in patients with acute septic inflammation whereas no variation appeared in patients with metastatic breast cancer. We also studied the variations of alpha 1-antichymotrypsin microheterogeneity in sera from patients with giant-cell arteritis and/or polymyalgia rheumatica before and during treatment with glucocorticoids.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Glycoforms of serum alpha 1-antichymotrypsin studied by immunoaffino-electrophoresis. From the fundamental aspect to clinical applications]. 175 31

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

The investigation concerned 33 systemic lupus erythematosus (SLE) patients assigned to three groups representing mild SLE, more severe extra renal SLE, and SLE with significant renal involvement. In patients with extrarenal disease, the inflammatory plasma protein response was often pronounced during exacerbation, as evidenced by markedly increased concentrations of C-reactive protein (CRP), alpha 1-antichymotrypsin, alpha 1-antitrypsin, and orosomucoid. CRP responses were rare in patients with renal involvement, despite the increased concentrations of other acute-phase reactants in some of these patients. Superimposed bacterial infections were not clearly distinguished by raised CRP concentrations. The classical pathway of complement was activated in all patients during exacerbation, as indicated by increased concentrations of C1r-C1s-C1 inactivator complexes and C2a fragments. C1, C2, and probably also C3 activation varied according to the amounts of circulating C1q-binding immune complexes, as measured by solid-phase assay. Manifest hypocomplementemia was usually associated with glomerulonephritis. Participation of complement components in the inflammatory plasma protein response apparently counteracted the development of hypocomplementemia in many patients with extrarenal SLE. Circulating C3d was detected in all patients during exacerbation of renal disease and in most patients with severe extrarenal manifestations. Inverse relationships were found between immunochemical C2 concentrations and the percentage of cleaved C2 and between C3 and C3d. There was no appreciable consumption of factors B and D and properdin of the alternative pathway in the patients. High concentrations of factor D, a low molecular weight protein, were exclusively found in patients with renal involvement and could be ascribed to retention due to reduced glomerular filtration.
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PMID:Complement components, complement activation, and acute phase response in systemic lupus erythematosus. 608 33

We sought to investigate the influence of interleukin-10 (IL-10) and IL-6 on the acute phase proteins (APP) in systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). IL-10, IL-6, Creactive protein (CRP), alpha-1-acid glycoprotein (AGP), and alpha1 antichymotrypsin (ACT) serum levels were determined in one hundred-eight patients (71 with SLE, 37 with RA). Quantification of the serum IL-10 level showed increased levels in SLE and RA patients as compared to healthy controls. Serum IL-6 level was found to be elevated in SLE and RA patients. A correlation between IL-10 and IL-6 serum level was found only in SLE. CRP and AGP serum levels were increased in RA as compared to controls, whereas in SLE only AGP was found elevated. A statistically significant correlation between IL-6 serum level and CRP, AGP and ACT was found only in RA. No correlation between IL-10 and serum level of CRP, AGP and ACT was established. Since IL-10 has a potent immunosuppressive activity, we expected it to be negatively correlated with APP levels. Surprisingly, IL-10 did not correlate with APP either in SLE or RA patients. However, the elevation of IL-10 serum levels in SLE and RA and the correlation between IL-10 and IL-6 in SLE may suggest that IL-10 may play a central role in inflammatory connective tissue diseases.
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PMID:Interleukin-10 and interleukin-6 in lupus erythematosus and rheumatoid arthritis, correlations with acute phase proteins. 918 65

Gliomas have been classified into different molecular subtypes based on their molecular features. To explore the prognostic factors of different subtypes of gliomas, we performed a univariate survival analysis based on the RNA-seq data of 653 patients obtained from The Cancer Genome Atlas. We identified 12205 (20.18%), 6125 (10.13%) and 5206 (8.61%) genes associated with the overall survival (OS) of the IDH-wildtype, IDH-mutation 1p/19q intact and IDH-mutation 1p/19q codeletion gliomas, respectively. Pathway enrichment analysis revealed that OS related genes were mainly involved in alcoholism, systemic lupus erythematosus, hematopoietic cell lineage and diabetes. The OS related genes were further selected using Lasso regression, and three prognostic risk score models were constructed to effectively predict the OS of the patients with different subtypes of gliomas. In total, 76 signature genes were identified and were selected to construct the three models. Moreover, neither of the 76 genes overlapped between different models, which suggested the enormous difference among the three subtypes, although some signature genes (SERPINA5, RP11.229A12.2 and RP11.62F24.2) were also identified as the OS related genes in different glioma subtypes. Interestingly, five genes (RP11.229A12.2, RP11.62F24.2, C3orf67, RP11.275H4.1 and TBX3) played opposing roles (protective or risk factor) in different subtypes. Additionally, the prognosis models consisted of a substantial proportion of non-coding RNA (58.74%, 70.13% and 58.11% in the IDH-wildtype, IDH-mutation 1p/19q intact and IDH-mutation 1p/19q codeletion). Furthermore, multivariate analysis integrating clinical variables demonstrated that risk group predicted by the prognostic models was an independent prognostic factor for gliomas. In conclusion, we have constructed and validated three models that have the potential to predict the prognosis of glioma patients. The genes and pathways identified in this study require further investigation for their underlying mechanisms and potential clinical significance in improving the OS of the glioma patients.
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PMID:Survival Risk Prediction Models of Gliomas Based on IDH and 1p/19q. 3248 48