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)

Ki antigen from rabbit thymus extract was purified by ammonium sulfate precipitation, anti-Ki affinity chromatography, and high pressure liquid chromatography gel filtration. The purified Ki antigen gave a single polypeptide with an MW of 32,000 by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and it specifically reacted with anti-Ki antibody by immunoblotting. The isoelectric point of the Ki antigen was found by isoelectric focusing to be 4.3. An enzyme-linked immunosorbent assay using the purified Ki antigen was established, and the clinical significance of the anti-Ki antibody in systemic lupus erythematosus (SLE) was studied. Thirty of 140 patients with SLE (21.4%) had anti-Ki antibody by enzyme-linked immunosorbent assay, whereas 11 (7.9%) were positive by double immunodiffusion. Analysis of clinical and serologic data on patients with SLE suggested a higher prevalence of central nervous system involvement in patients with anti-Ki antibody.
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PMID:Purification and characterization of Ki antigen and detection of anti-Ki antibody by enzyme-linked immunosorbent assay in patients with systemic lupus erythematosus. 259 10

We evaluated the effect of indomethacin on renal function in a sodium-restricted state in control subjects and in patients with systemic lupus erythematosus (SLE) without major disease activity and with normal or only slightly impaired glomerular filtration rate (GFR). In the patients with SLE indomethacin 150 mg daily induced a fall in GFR of mean 15.8%, while effective renal plasma flow remained constant. Neither effective renal plasma flow, nor GFR changed significantly in the controls. One should be aware that nonsteroidal anti-inflammatory drugs (NSAID) may decrease GFR in SLE, also in patients without disease activity and with normal or only slightly impaired GFR. As effective renal plasma flow remained constant, it is suggested that the indomethacin-induced fall in GFR in SLE is caused by mesangial contraction.
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PMID:Renal effects of indomethacin in patients with systemic lupus erythematosus. 267 8

The proliferative activity of peripheral blood mononuclear cells (PBMN) from patients with systemic lupus erythematosus (SLE) activated by sodium periodate (NaIO4) is greatly diminished. The effect of the cytokines Interleukin-1 (IL-1) and Interleukin-2 (IL-2) on the NaIO4 reaction was investigated. Addition of IL-1 resulted in partial restoration of the reaction of SLE PBMN to NaIO4, and a similar effect was demonstrated in the presence of phorbol myristate acetate (PMA). Addition of IL-2 to NaIO4 activated SLE PBMN, however, caused a marked improvement in their proliferative activity. The presence of indomethacin resulted in only a slight increase in [3H]thymidine incorporation by the NaIO4-treated SLE cells. The results suggest that the defect in the response of SLE PBMN cells to NaIO4 is due to inadequate availability of IL-1 and IL-2. Excessive production of prostaglandin in SLE might also contribute to the defective response to NaIO4 but does not appear to play a major role.
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PMID:Modulation of the sodium periodate (NaIO4) response in systemic lupus erythematosus (SLE): effect of interleukin-1 (IL-1), interleukin-2 (IL-2), phorbol myristate acetate (PMA), and indomethacin. 298 Nov 69

It has been anticipated that type C oncornaviruses, which participate in the pathogenesis of murine systemic lupus erythematosus (SLE), would be found to have a role in the development of SLE in humans. In studies of tissues from SLE patients, type C-related proteins have been identified. Using information obtained on the recent isolation of the human T cell leukemia virus (HTLV), together with that from studies of murine SLE, we attempted to clarify the role of antibodies to HTLV in the pathogenesis of human SLE. Using a solid-phase enzyme-linked immunosorbent assay and sodium dodecyl sulfate-polyacrylamide gel electrophoretic techniques, we were unable to find evidence of the participation of antibodies to HTLV proteins in the development of human SLE.
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PMID:Antibodies to human T cell leukemia virus are absent in patients with systemic lupus erythematosus. 298 71

Cold-reactive lymphocytotoxic autoantibodies are present in the serum of most patients with active systemic lupus erythematosus (SLE) and may be important for the development of the lymphopenia and T cell dysfunction characteristic of this disorder. Neither the mechanisms of autoantibody action in this regard, nor the nature of the relevant T cell membrane target molecules have been defined, however. In the present investigation, preincubation of T cells with SLE serum at 37 degrees C reduced their reactivity with SLE IgM anti-lymphocyte autoantibodies, as demonstrated by indirect immunofluorescence and complement-dependent cytotoxicity. Modulation was restricted to SLE IgM autoantibody-reactive antigen; monoclonal antibody staining of various T cell differentiation and activation antigens remained unchanged. Loss of antigen from the surface membrane was rapid, but transient. A nadir was reached after approximately 120 min of 37 degrees C incubation, followed by essentially complete reexpression of antigen several hours later. Although modulation occurred spontaneously at 37 degrees C in the absence of SLE serum, loss of antigen was enhanced by IgM anti-lymphocyte autoantibodies, despite their low thermal amplitude. Modulation was inhibited by sodium azide, by fixation of cells with paraformaldehyde, and by low incubation temperatures. Colchicine and cytochalasin D had no effect on this process, suggesting that the integrity of the cytoskeleton was not essential. Cycloheximide did not prevent loss of antigen, but inhibited its reexpression. In experiments to determine the fate of modulated antigen, both intracytoplasmic accumulation and shedding from the cell surface were demonstrated. Only shedding was increased by the presence of anti-lymphocyte antibodies, however. These studies delineate modulation of T cell membrane antigen as a new mechanism for anti-lymphocyte autoantibody action in SLE. The occurrence of modulation at physiologic temperatures in vitro suggests that a similar phenomenon of potential relevance to T cell dysfunction may obtain in patients with this disorder.
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PMID:Modulation of IgM anti-lymphocyte antibody-reactive T cell surface antigens in systemic lupus erythematosus. 300 14

P3HR-1 and Ramos cells induced with sodium butyrate and 12-O-tetradecanoylphorbol 13-acetate were used in the protein immunoblot technique to identify Epstein-Barr virus (EBV)-specific antibodies present in sera from clinically normal individuals and patients with systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) and infectious mononucleosis (IM). Sixteen EBV-specific polypeptides were detected ranging in mol. wt. from 22,000 (22K) to 140K. Many of the sera contained antibodies to different subsets of these antigens, and a high proportion expressed autoantibodies which reacted with cellular components from an EBV genome-negative cell line. About 50% of the sera from each category reacted with the 44K to 48K and 36K and 38K early antigen (EA) components. A high proportion of the SLE sera (64%) were found to contain anti-EA antibodies, suggesting an association between EBV and SLE. Almost all of the EBV-seropositive sera examined contained antibodies against a 22K late antigen, but none of the sera from IM patients reacted with this polypeptide.
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PMID:Reactions of sera from patients with rheumatoid arthritis, systemic lupus erythematosus and infectious mononucleosis to Epstein-Barr virus-induced polypeptides. 302 Jan 61

Bradykinin is degraded in human plasma by a carboxypeptidase to yield desArg9-bradykinin (DBK) which is then digested by angiotensin-converting enzyme (ACE) to the pentapeptide Arg-Pro-Pro-Gly-Phe and the tripeptide Ser-Pro-Phe. We have studied the rate of kinin degradation by each of these enzymes in patients with rheumatoid arthritis (RA) and with systemic lupus erythematosus (SLE), compared with the degradation rate in degenerative joint disease and normal subjects. Carboxypeptidase activity was the same in all individuals, but ACE activity was increased in the RA and SLE patients. We examined the effects of aspirin, sodium salicylate, auranofin, penicillamine, and corticosteroids on kinin metabolism, and all of these were marked inhibitors of ACE; however, only penicillamine had any demonstrable inhibition of carboxypeptidase. These observations suggest rapid degradation of DBK in patients with untreated RA and SLE, whereas drugs utilized in therapy have the opposite effects. Studies to examine the role of DBK in disease manifestations are in progress.
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PMID:Assessment of kininases in rheumatic diseases and the effect of therapeutic agents. 303 Mar 35

We prospectively evaluated 30 patients who presented with active systemic lupus erythematosus (SLE) for the presence of tubular abnormalities. All patients fulfilled the American Rheumatology Association criteria for SLE. When appropriate, a renal biopsy was performed. Of the 30 patients studied, 12 had no abnormal tubular study results, whereas 18 patients had some form of defect in the handling of potassium, sodium, or hydrogen ions. Eight patients had distal renal tubular acidosis (dRTA) due to an isolated proton secretory defect. Five had dRTA of the gradient or acid back-leak type. Two had an unresponsive voltage-dependent form of dRTA; one had a responsive voltage-dependent form of dRTA. One individual had hyporeninemic hypoaldosteronism and one had dRTA plus hypoaldosteronism. Clinically, patients with the abnormal tubular study results more often presented with nephritis or nephrotic sediment, peripheral edema, or anemia. Renal biopsies failed to demonstrate any difference in glomerular histologic findings and calculated activity, chronicity, or interstitial indexes. We conclude that SLE may be associated with a variety of tubular defects.
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PMID:Occurrence of renal tubular dysfunction in lupus nephritis. 303 79

We describe the coagulopathy of a 65-year-old woman with a thrombotic disorder associated with dysfibrinogenemia and lupus anticoagulant (LA). The patient's prothrombin time (PT), partial thromboplastin time (PTT), thrombin time (TT), and batroxobin time were prolonged and could not be corrected by mixing with equal volumes of normal plasma. Fibrinogen quantitation showed approximately twice as much immunoreactive as thrombin-clottable protein. The batroxobin and thrombin clotting times of the patient's isolated fibrinogen were prolonged and could not be corrected by mixture with normal fibrinogen. Turbidimetrically assessed fibrin monomer aggregation in response to thrombin, ancrod, or batroxobin and fibrin monomer reaggregation experiments disclosed clearly delayed onset and a lower maximum opacity. In other turbidimetric and clotting-time experiments, the patient's fibrinogen displayed a dose-dependent inhibition of the reaggregation of normal fibrin. Fibrinopeptide A and B release rates and sialic acid content were normal. Assessed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) of reduced samples, the subunit structure of the patient's fibrinogen and its fully cross-linked fibrin was normal. The presence of LA was established by two techniques, the blood thromboplastin inhibition test and the platelet neutralization procedure (PNP). A positive PNP could not be produced by mixing afibrinogenemic plasma with the patient's purified fibrinogen. The patient's inactivated serum and her isolated IgG prolonged the PT and PTT of normal plasma but showed no inhibitory effect on the clotting of purified normal fibrinogen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dysfibrinogenemia and lupus anticoagulant in a patient with recurrent thrombosis. 311 49

IgG antilymphocyte antibodies preferentially reacting with phytohemagglutinin (PHA) activated peripheral blood lymphocytes (PBL) and an adult T cell leukemia cell line were detected in 70.6% sera from patients with systemic lupus erythematosus (SLE), using a fluorescence activated cell sorter (FACS). In the sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) analysis, 2 major peaks with an apparent molecular weight 60,000 to 65,000 Da and about 40,000 Da were observed in the membrane glycoprotein fractions of both PHA activated PBL and an adult T cell leukemia cell line. From the result of sequential coprecipitation analysis of SDS-PAGE between SLE serum, antiinterleukin-2 (IL-2) receptor antibody (anti-Tac antibody) and anti-Ia antibody, the reactive antigen on the activated PBL and an adult T cell leukemia cell line proved to be an identical molecule of the IL-2 receptor on these cells. The role of this autoantibody in the modulation of T cell mediated immunity in patients with SLE is discussed.
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PMID:Antibody to activated lymphocytes in patients with systemic lupus erythematosus. 312 75


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