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PubMed1977

In vivo fixation of immune complexes on polymorphonuclear cells and release of neutrophil cationic proteins in systemic lupus erythematosus (SLE).

Neutrophils (PMN) appear to be involved in inflammatory phenomena as a result of direct interaction with immune complexes (IC). In SLE glomerulonephritis IC are fixed in vivo on the PMN surface through the receptors for FC fragments of complexed immunoglobulins and complement. Phagocytic properties are lost and immunological lysosomal release in vitro is markedly reduced by virtue of receptor occupation. The elimination of neutrophil cationic proteins (NCP) in urine is an expression of PMN lysosomal constituent release.

Antigen-Antibody Complex↗
PubMed1976

Fibroblast lysis by lymphocytes from normal persons and SLE patients on short-term cultures.

Lymphocytes from thirty-six normal individuals of both sexes with ages ranging from 4-89 years were tested for their cytotoxic activity against short term cluters of fibroblasts from nine foetal umbilical cords and nine adult skin samples. Wide variability in the amount of fibroblast lysis was observed. Adult male lymphocytes caused significantly higher lytic activity than lymphocytes of adult females against both types of targets. Cell-mediated target cell reduction was not confined to allogeneic target cells. There was also killing of autochthonous cultured fibroblasts. Some individuals' sera inhibited the fibroblast lytic activity of their own lymphocytes. These cell-mediated reactions are directed against unknown antigenic specifications, probably not histocompatibility antigens, and give evidence of the problem of how to measure normal controls in the microcytotoxicity test in allogeneic human testing. Both autochthonous and allogeneic target cell lysis were also observed in SLE patients.

Adolescent↗
PubMed1983

Lymphocyte subtypes in patients with atopic eczema, protein calorie malnutrition, SLE and liver disease.

Peripheral blood lymphocytes from patients with protein calorie malnutrition, atopic eczema, systemic lupus erythematosus and in three groups of patients with liver disease, were characterized by reactivity with monoclonal antibodies to the surface antigens of helper-inducer (OKT4) and suppressor-cytotoxic (OKT8) T cell subsets and to a common T cell antigen (OKT3). The protein calorie malnutrition group showed a considerable decrease in all subsets while patients with atopic eczema displayed an increase in the total number of OKT3+ cells, attributable primarily to an increase in the OKT4+ cell population with the OKT8+ cells remaining within normal values. In the SLE group, only 3 of the 16 patients had OKT8+ numbers below that of normal controls, whereas the mean number of OKT4+ cells in the group was less than normal controls. The striking feature of patients with liver disease, was the altered ratio of OKT4+ to OKT8+ cells in the hepatocellular carcinoma and amebic liver abscess groups due primarily to decreased OKT4+ and raised OKT8+ cell subpopulations.

Antibodies, Monoclonal↗
PubMedDate not supplied

Antibodies to dsDNA and ssDNA in the immunoglobulin classes IgG and IgM: prognostic value in the course of SLE.

Antibodies to dsDNA of the IgG-class show a strong association with disease activity in the course of systemic lupus erythematosus (SLE). Of 22 patients with low dsDNA-levels only one had an exacerbation. In 8 patients a rise of IgG-dsDNA antibodies to high levels occurred, followed by an exacerbation in 7 of them. In 6 of these 7 patients the IgG-dsDNA antibodies had a prognostic value by rising into high ranges 2-12 weeks before the exacerbation. IgG-ssDNA antibodies showed only a weak association to the clinical course. IgM antibodies to dsDNA as well as to ssDNA did not correlate with the clinical activity at all.

Antibodies, Antinuclear↗
PubMed1983

Autoimmunity and laboratory testing for systemic lupus erythematosus (SLE) and allied diseases.

Thus, we can see that in our prototype autoimmune disease SLE, many different autoantibodies can be present. The laboratory tests for detecting these antibodies are important in the diagnosis and management of this group of diseases. Current research has focused on the defective T suppressor cell function, and the recent exciting developments in this area are certain to open up new laboratory approaches for studying these diseases.

Antibodies, Antinuclear↗
PubMed1983

Shrinking lung syndrome in SLE--a clinical pathologic study.

A patient with systemic lupus erythematosus (SLE) who developed shrinking lung syndrome during the course of her disease is described. Postmortem findings of diffuse diaphragmatic fibrosis support the hypothesis of an extrapulmonary restrictive etiology in this unusual condition.

Female↗
PubMed1982

Pulse methylprednisolone in SLE.

Insufficient information is available about the effectiveness of high-dose intravenous corticosteroid treatment in non-renal SLE to determine whether it provides better management of the disease. Issues of steroid preparation, dose and frequency have not been addressed. Significant short-term complications appear to be minimal; the question of long-term effects on avascular necrosis may not be answerable since most patients also receive oral corticosteroids at some time during their course. No large randomized controlled trial of pulse IV-MP in lupus nephritis is available. Ideally, such a trial would include randomization with stratification according to important prognostic variables. Previous studies of other agents have been hampered by lack of agreement about both the identification of relevant prognostic variables and the selection of 'significant' measures of outcome. The observation that patients with recent deterioration in glomerular filtration rate are more likely to improve after IV-MP may form the basis for stratification in a controlled trial of the comparative efficacy of IV-MP and other forms of treatment. However, lack of improvement in glomerular filtration rate among patients without recent deterioration in function may reflect the inadequacy of our outcome measures rather than a true lack of beneficial effect for the patient.

Bacterial Infections↗
PubMed1981

[Ulnar nerve-hypothenar muscle H-reflex in a child with SLE (author's transl)].

In the hypothenars of a 14 years old boy with SLE an abnormal H-reflex could be elicited by ulnar nerve stimulation. Beyond infancy this phenomenon has only been described in patients with lesions of the higher cervical spinal cord and/or the lower brain stem and in children with Sydenham's chorea. There might be reason to assume, that in alike auto-immune disorders the search for an H-reflex in the hypothenar might be useful in detection of cerebral involvement.

Adolescent↗
PubMed1982

Antibodies to extractable nuclear antigens in 173 patients with DNA-binding positive SLE: an association between antibodies to ribonucleoprotein and Sm antigens observed by counterimmunoelectrophoresis.

Sera from 173 patients with systemic lupus erythematosus (SLE) were examined for antibodies to extractable nuclear antigens (ENA) by counterimmunoelectrophoresis (CIE). Antibodies to four major constituents were identified and their frequencies noted as follows: anti-RNP (28%), anti-Sm (10%), anti-Ro (24%) and anti-La (9%). In addition to these a number of uncharacterised antigens were also noted. Using the CIE method we found that in cases where anti-Sm was present it was always accompanied by anti-RNP. Associations between these two antibodies have been noted previously, and many theories have been put forward in explanation. In this study a simple interpretation of the results is offered based on current knowledge of the molecular structure of Sm and RNP antigens.

Animals↗
PubMed1982

Kinetic studies of phagocytosis. III. The complement-dependent opsonic and anti-opsonic effects of normal and sle sera.

The influence of serum on phagocytosis related to the complement system was examined by means of a kinetic phagocytosis method using IgG-coated particles, isolated polymorphonuclear neutrophil leucocytes (PMNs), fresh serum, in vitro activated sera and in vivo activated sera. The previously described opsonic properties of C3b and C4b were confirmed by the enhancement of phagocytic rate by the opsonization of IgG particles with C3 and C4. An anti-opsonic effect of serum was revealed by the initial inhibition of PMN phagocytosis of IgG-coated particles in the presence of fresh serum. In vitro activated norma fresh serum and in vivo activated SLE sera mediated a prolonged or even irreversible inhibition of phagocytosis dependent on the degree of complement activation. Investigation of this anti-opsonic effect of serum, which was heat-labile, suggested that it was caused by an inhibition of the interaction between the Fc receptor and IgG mediated by the C1q component of the C1 complex.

Complement Activating Enzymes↗
PubMed1980

Loss of monocyte membrane receptors in patients with SLE.

Following an 80-min cold treatment of monocytes and their subsequent heating at 37 degrees C a part of the Fc and C3 receptors is shed from the cells into the serum-free medium. However, while the reduced expression of cell membrane Fc receptors is regenerated at 37 degrees C in 4-8 hr, that of the C3 receptors is not. Initially, the Fc receptor expression of monocytes for patients with SLE is greater than that of controls and after shedding it increases to the level of controls at 37 degrees C in 4-8 hr. The expression and the regeneration of C3 receptors are equivalent to those of controls. The phagocytic ability of patient monocytes is lower than that of controls and the difference also remains after heat treatment.

Female↗
PubMedDate not supplied

Apoptosis in SLE--too little or too much?

Cells of the immune system are, most likely, programmed to die unless recruited into an immune response. An active cell death program may also be induced by a variety of soluble and surface signals, many of which have only recently been recognized. The importance of these pathways in maintaining tolerance is highlighted by the development of lupus-like diseases in three different mouse strains that have spontaneous mutations in the Fas/APO-1 receptor or its ligand. The known function of Fas/APO-1 in signalling apoptosis explains the persistence of self reactive cells in lpr mice although it is unclear, at present, whether Fas defects effect both central and peripheral tolerance. Whereas Fas/APO-1 receptor expression appears to be normal in humans with SLE, other defects in the Fas/APO-1 pathway or other key molecules in the cell death survival require further study.

Animals↗
PubMed1995

SLE-like autoantibodies and Sjögren's syndrome-like lymphoproliferation in TGF-beta knockout mice.

Mice bearing the TGF-beta 1 null mutation (-/-) develop lymphoid infiltrates in the heart, lungs, salivary glands, and other organs similar to those seen in the pseudolymphoma of Sjögren's Syndrome. We studied sera from -/- mice and found elevated Ab levels to dsDNA, ssDNA, and Sm ribonucleoprotein. No Abs to SSA/Ro or SSB/La and no IgM rheumatoid factor were found. Serum autoantibodies were predominately IgG and were specific as shown by ELISA inhibition studies. Antinuclear Ab patterns on Western blots varied from one mouse to the next, indicating a random process responsible for the diversity. Wild-type and heterozygote mice had no autoantibodies. Ig glomerular deposits were found in -/- mice, indicating that these autoantibodies may be pathogenic. Treatment of -/- mice with dexamethasone or TGF-beta 1 failed to suppress autoantibody production. These mice represent an overlap combining the autoimmune serology of SLE with the tissue infiltrates of SS. Our results support the concept that TGF-beta 1 is an important naturally occurring immunosuppressive cytokine whose absence can lead to a systemic autoimmune disease.

Animals↗
PubMed1994

Mycobacteria precipitate an SLE-like syndrome in diabetes-prone NOD mice.

Non-obese diabetic (NOD) mice spontaneously develop organ-specific autoimmunity and are widely used as a model for diabetes. Aged NOD mice also exhibit some features of non-organ-specific autoimmune rheumatic disease such as anti-nuclear antibodies and late-onset haemolytic anaemia. Here, we report that a single dose of 2.6 x 10(7) heat-killed bacillus Calmette-Guérin (BCG) i.v. in 8-week-old NOD mice prevented diabetes but precipitated a syndrome similar to systemic lupus erythematosus (SLE). Treated mice developed haemolytic anaemia, anti-DNA and anti-Sm anti-nuclear autoantibodies and an increased severity of sialadenitis. Perivascular lymphocytic infiltration in the kidneys and glomerular immune complex deposition were also found. The action of BCG appeared to be mediated by an adjuvant-like activity as treated mice showed a substantial increase in reticuloendothelial cell function and enhanced antigen presentation capacity.

Anemia, Hemolytic, Autoimmune↗
PubMedDate not supplied

Study of C4A mRNA in mononuclear blood cells from a patient with SLE and C4A homozygous deficiency without C4A gene deletion.

C4A null alleles (C4AQ0) have an increased frequency in SLE patients. Surprisingly some of them have no detectable gene deletion. In order to characterize the level of the defect in such patients, we used a RT-PCR/nested PCR technique and detected the presence of C4A mRNA in normal amounts. Since maturation abnormalities are almost always accompanied by a decrease in mRNA concentration, this result suggests that the defect may be located at the translational level.

Base Sequence↗
PubMed1994

C3 nephritic factor and SLE: report of four cases and review of the literature.

We present four patients with C3 nephritic factor associated with partial lipodystrophy and/or mesangiocapillary glomerulonephritis type II. Each of these patients subsequently developed features of SLE, with an onset between 2 and 24 years after the development of the lipodystrophy or glomerulonephritis. All four patients had antinuclear antibodies and three of the four had anti-Ro antibodies. These patients bring to six the number of reported cases of this association. Possible explanations for the link between these two conditions are discussed.

Adult↗