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)

Glomiform inclusions, also called tubular arrays in endoplasmic reticulum, are found in the epithelial cells of glandular tissues of a patient with systemic lupus erythematosus, a patient with Reye's syndrome, and a dog. Their three dimensional structure is interpreted as a skein of contorted tubules of endoplasmic reticulum. Fibrillar inclusions found in the pancreatic acinar cells of two patients are believed to represent altered zymogen granules.
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PMID:Glomiform and fibrillar cytoplasmic inclusions. 17 77

The fine structures of the red pulp of the spleen and the liver of a patient with autoimmune hemolytic anemia, neutropenia and thrombocytopenia associated with systemic lupus erythematosus are described. The red blood cells were phagocytized in toto by the splenic macrophages. These also contained neutrophils and platelets in various stages of degradation. Sinus endothelial cells revealed occasional erythrophagocytosis. The Kupffer cells in the liver occasionally contained red cells and platelets. These morphological findings and marked improvement of hematological abnormalities following splenectomy suggested that the spleen was the major site of destruction of blood cells. Undulating tubules associated with the endoplasmic reticulum were present in the sinus endothelial cells of the spleen.
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PMID:Fine structure of the spleen in autoimmune hemolytic anemia associated with systemic lupus erythematosus. 63 98

Electron microscopic examinations revealed the presence of myxovirus-like tubular structures, 200A in diameter, in the endothelial cytoplasm of the glomeruli in four dogs with chronic interstitial nephritis and in one healthy control dog. The structures were found inside the endoplasmic reticulum and in some longitudinal sections, the tubuli seemed to have a helical or spiral substructure. The morphology and cellular localization of the structures resembled those seen in systemic lupus erythematosus in man, and in cultures of cells from tissue infected with canine distemper. Precipitating canine distemper virus antibodies were not in evidence in dogs in which such structures were demonstrable by electron microscopy while these antibodies were found in other dogs.
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PMID:Myxovirus-like structures in the glomerular endothelial cell cytoplasm in canine nephritis. 115 3

Cytoplasmic inclusions of great complexity are encountered in an undifferentiated sarcoma of a 67-year-old woman. The tumor arising in adipose tissue between muscles of the parspinous musculature contains inclusions in most tumor cells represented by four different morphologic types. Two are intracisternal, designated microtubular reticular structure (TRS) and tubular confronting cisternae (TCC). Two others are cytoplasmic and consist of crystalline microtubular arrays and of confronting cisternal complexes of smooth endoplasmic reticulum (SER). This latter is uniquely complex and not found in previous descriptions. Tumors of mesenchymal origin and experimental virus-induced tumors are known to contain short segments of confronting cisternae and TRS. Tubuloreticular structures and TCC are well documented in cases of lupus, in human immunodeficiency virus infections, in T-cell leukemia, and in experimental viral hepatitis in chimpanzees. The patient presented has none of the coincidental pathologic condition associated with occurrence of TRS and TCC. The morphology of the inclusions and their relationships are illustrated although their biological significance remains obscure.
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PMID:Soft tissue sarcoma with complex membranous and microtubular inclusions. 166 96

By flow cytometry analysis we could show a decreased expression of Fc gamma receptor type III (Fc gamma RIII) on granulocytes of a patient with systemic lupus erythematosus (SLE). Therefore, we constructed a leukocyte cDNA library from this patient with the aim of investigating this defect on the molecular level. Using an Fc gamma RIII cDNA probe we isolated 15 Fc gamma RIII cDNA clones, which were all characterized by sequencing. Our sequence data revealed that the patient was heterozygous for Fc gamma RIII (NA-1/NA-2). Only clone 5 (NA-2) was a full-length cDNA clone. In contrast to the wild-type Fc gamma RIII the signal sequence is mutated, lacking the hydrophobic region essential for co-translational transport across the endoplasmic reticulum membrane. The predicted transport defect leading to the lack of membrane expression could be confirmed by immunofluorescence staining after expression of this cDNA clone in BHK cells. The cDNA clones 6 and 8 (NA-1) lack the first 45 bp of the signal sequence, but considering the flow cytometry data the signal sequence must be functional allowing the membrane expression of this receptor allele. The part of the cDNA sequence of all isolated clones coding the mature Fc gamma RIII is identical to the wild-type sequence. Therefore, we conclude that the decreased expression of Fc gamma RIII on granulocytes of this SLE patient is due to the transport defect of one of the receptor alleles.
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PMID:Molecular basis of IgG Fc receptor III defect in a patient with systemic lupus erythematosus. 182 62

The presence of the antiperinuclear factor, an autoantibody that recognizes cytoplasmic antigens, was detected in sera from patients with rheumatoid arthritis (59%), seronegative rheumatoid arthritis (36%), systemic lupus erythematosus (46%), systemic sclerosis (26%), and in nonautoimmune controls (10%). The antigenic perinuclear granules were found in the stratum intermedium layer of the buccal mucosa. Granules exhibited histologic features of nucleoproteins, stained for ribonucleoprotein, and showed the ultrastructural characteristics of aggregated rough endoplasmic reticulum. The antiperinuclear factor may recognize a common autoantigen in connective tissue disease.
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PMID:Histologic and electron microscopic characterization of the antiperinuclear factor antigen. 219 59

Tubuloreticular inclusions (TRI) have been observed in the rough endoplasmic reticulum of blood lymphocytes and monocytes in two cases of Reye's syndrome initiated by influenza infections. Tubuloreticular inclusions are seen in these mononuclear leukocytes during the acute phase of illness, but not during convalescence. Since TRI have been demonstrated in peripheral mononuclear leukocytes in patients with acquired immunodeficiency syndrome, systemic lupus erythematosus, and certain viral infections including T-cell leukemia, it may be that the finding of TRI in Reye's syndrome reflects a viral infection and/or immune dysfunction, if such association is not proved to be fortuitous.
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PMID:Leukocyte tubuloreticular inclusions in Reye's syndrome. 258 24

In a murine lupus model, the kidneys of 42 MRL mice of different age groups (substrains MRL/Mp-lpr/lp and -+/+) were studied by light and transmission electron microscopy. The results demonstrate the ultrastructural feature of the mesangial-proliferative glomerulonephritis which is one of the observed forms of glomerulonephritis. The most important alterations are a severe proliferation of mesangial cells (with an increase in rough endoplasmic reticulum and mitochondria) and electron dense deposits in different sites of the glomerular basement membrane (subepithelial, subendothelial, intramembranous). These deposits are proposed to be immune complexes. Osmiophilic intracytoplasmic inclusions of the mesangial cells are indications of an altered renin production. Alterations of the glomerular epithelial cells are characterized by fusions of the epithelial pedicles, an increase of microvilli and intracytoplasmic concentrations of electron dense material which are also proposed to be immune complex deposits. The morphological feature of the mesangial-proliferative glomerulonephritis is completed by an activation and focal edema of endothelial cells. The described alterations are discussed and compared with findings in other species.
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PMID:[Electron microscopic structure of mesangioproliferative glomerulonephritis (MesPGN) in animals]. 265 80

Human alpha interferons (IFN-a) cause a reorganization of internal cell membranes into tubuloreticular inclusions (TRI). Morphogenesis and cytochemistry indicate a pre-Golgi intracisternal origin from the endoplasmic reticulum. Clinically, TRI formation in human blood mononuclear cells correlates with systemic IFN-a treatment or with endogenous overproduction of IFN-a in viral or autoimmune diseases (e.g., rubella syndrome, AIDS, systemic lupus erythematosus). In vitro, TRI formation can be produced by treatment of Daudi lymphoblasts or vascular endothelial cells with IFN-a, and is blocked by actinomycin-D. In Daudi lymphoblasts or vascular endothelial cell cultures, TRI formation parallels induction of 2'-5' A synthetase, inhibition of thymidine kinase and growth inhibition; however, heavy water treatment of Daudi cells prevented TRI formation while induction of 2'-5' A synthetase and growth inhibition persisted. TRI formation was dissociated from IFN-a antiproliferative activity in a mutant clone of Daudi lymphoblasts. Decreased glycoprotein biosynthesis and increased phospholipid biosynthesis may accompany progressive TRI accumulation.
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PMID:Tubuloreticular reorganization of cytomembranes in cells treated with human alpha interferons--a review. 307 Jul 35

Sera with anti-mitochondrial autoantibodies detected by indirect immunofluorescence and/or enzyme-linked immunosorbent assay (ELISA) were examined by immunoblotting against pig heart mitochondria. Seven types of reactions were defined, according to the pattern of the labelled bands. Type I sera reacted with 12 bands located within four zones. The most intensively labelled bands were located at 70, 67, 58, 63 and 43 kDa. Other types gave decreasing band numbers. When beef heart mitochondria were used, sera belonging to each of the above types had a profile of labelled bands which sometimes differed from those obtained with pig heart mitochondria. When the chloroform extracted F1-ATPase from beef heart mitochondria was used to prepare the immunoblots, primary biliary cirrhosis (PBC) sera with anti-mitochondria antibodies reacted with all the bands although zone A bands were less labelled. Rat liver mitochondria gave seven bands with type I sera among which the 57 and 35 kDa bands were specific for rat liver mitochondria, as shown by absorption tests. Sera of PBC patients were also tested in immunoblotting against rat liver subcellular fractions including mitoplasts, submitochondrial particles, inner membrane, outer membrane, matrix proteins and inter-membrane proteins. Antigenic bands of A and B zones were localized in the inner membrane and/or in the matrix proteins and the 35 kDa band in inter-membrane proteins. The outer membrane gave no reaction. The most frequent anti-mitochondrial autoantibody types in PBC were type II, then I, whilst for chronic active hepatitis type III was the most common. Type V was only seen in a patient suffering from a typical PBC. Some sera from patients with syphilis, collagenous colitis or progressive systemic sclerosis labelled one or two bands distinct from those labelled by the PBC sera. Sera from patients with drug-induced hepatitis with endoplasmic reticulum antibodies and with systemic lupus erythematosus were generally found negative by immunoblotting.
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PMID:Use of immunoblotting to characterize the mitochondrial antigens recognized by anti-mitochondrial autoantibodies. 317 Nov 87


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