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PubMed1989

Dyslipoproteinemia in murine systemic lupus erythematosus.

Dyslipoproteinemia, a feature of systemic lupus erythematosus may contribute to premature atherosclerosis. In order to develop an experimental model for this dyslipoproteinemia we measured plasma concentrations of lipoproteins in juvenile NZB/W (lupus) and NZB/B (control) mice. Additionally to evaluate the effects of a diet rich in n - 3 fatty acids we measured lipoprotein concentrations in mice on normal or menhaden oil-enriched diets. The lupus mice had elevated triglycerides compared to the controls, similar to that seen in human SLE patients (161 +/- 31 vs 113 +/- 13 mg/dl, P less than 0.003). In contrast, the menhaden oil diet fed NZB/W mice had triglycerides similar to the NZB/B control fed group. In the NZB/W murine SLE model, dyslipoproteinemia is an early sign of disease as has been shown in man, therefore this model will be useful in elucidating the mechanism of dyslipoproteinemia in SLE.

Animals↗
PubMed1982

Histologic and sialochemical findings indicating sicca syndrome in patients with systemic lupus erythematosus.

Twenty unselected patients with systemic lupus erythematosus (SLE) were investigated with respect to symptoms and signs of salivary gland involvement. Eight of them complained of xerostomia. Whole salivary flow was measured, parotid saliva was analyzed chemically, and palatal biopsy was performed to assess the degree of inflammatory infiltration in minor salivary glands. All but one of the patients showed signs of involvement on at least one of the tests and, as a group, the patients with SLE had significantly reduced values for salivary flow and increased concentrations of sodium, protein, and carbohydrates as compared to matched healthy controls.

Adult↗
PubMed1982

The pathogenesis of systemic lupus erythematosus.

Many investigators believe that systemic lupus erythematosus is an autoimmune disease, perhaps caused by inadequate suppressor T lymphocyte activity, which permits the activation of autoantibody producing B lymphocytes. This paper discusses the testable hypothesis that a superoxide-generating, chromosome aberration-inducing factor (clastogenic factor), present in the lymphocytes of lupus patients but absent from normals, is responsible for such a suppressor cell defect. Superoxide or activated oxygen species derived from it, such as hydroxyl radical, may be the molecular mediators of CF activity.

Chromosome Aberrations↗
PubMed2006

Systemic lupus erythematosus and pregnancy.

Women with systemic lupus erythematosus (SLE) face significant risks when embarking on a pregnancy, but attending a multidisciplinary clinic staffed by an experienced team can improve pregnancy outcome for women and their babies. Pregnancy in SLE should be planned and a management strategy should be agreed in full consultation with the patient, prior to conception. Pregnancy increases the likelihood of a lupus flare. It is not possible to predict when, or if, an individual patient will flare, although flare is more likely if disease has been active within 6 months of conception. Worsening of proteinuria in pregnancy could herald a lupus flare, but the differential diagnosis also includes the physiological response to pregnancy and pre-eclampsia. Corticosteroids, hydroxychloroquine and azathioprine are safe to use in pregnancy, with no adverse fetal effects reported despite many years of experience with their use. Correct identification of patients with antiphospholipid syndrome is important because treatment of affected women during pregnancy can improve fetal and maternal outcome. Neonatal SLE, although rare, carries a significant mortality and morbidity when the fetal heart is the targeted organ. Prophylaxis therapies, including treatment with intravenous immunoglobulin, await larger trials.

Female↗
PubMed2006

Abnormal intracellular distribution of NFAT1 in T lymphocytes from patients with systemic lupus erythematosus and characteristic clinical features.

Systemic lupus erythematosus (SLE) presents various clinical features; however, underlying mechanisms remain unclear. In the immunity of SLE, impaired T cell receptor (TCR) signaling and altered cytokine production are in the center of pathogenesis, although, little is known about NFAT (nuclear factor of activated T cells) in lupus T lymphocytes. TCR stimulation activates NFAT1 through Ca2+/calcineurin (Cn) pathway, facilitating nuclear translocation of NFAT1 from cytosol. Therefore, we investigated relationship of disease activity/features and intracellular NFAT1 localization in T lymphocytes from active lupus patients by fractionation. Results showed no significant relationship between disease activity and NFAT1 distribution. However, interestingly, we observed skewed NFAT1 distribution in pellet in patients with active lupus nephritis or pleuritis. In vitro cyclosporin A treatment suggested autonomously activated Ca2+/Cn pathway in lupus T lymphocytes. Considering these results, NFAT1 might be presenting the clinical heterogeneity in SLE.

Adult↗
PubMed2006

Rembrandt's Maria Bockenolle has a butterfly rash and digital deformities: overlapping syndrome of rheumatoid arthritis and systemic lupus erythematosus.

Rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) are the most common autoimmune disorders, although they each have very different pathophysiology. In general, RA is considered to be a Th1-mediated disease, while SLE is a Th2-mediated disease. Thus, their overlapping, in so called "rhupus", is a rare condition. In Rembrandt van Rijn's (1606-1669) portrait of the middle-aged Maria Bockenolle, we have what may be the earliest depiction of a case of rhupus syndrome: the coexistence of a butterfly rash and digital deformities. This suggests the possible historical importance of an RA epidemic which took place in the early 17th century.

Arthritis, Rheumatoid↗
PubMed1996

Undiagnosed systemic lupus erythematosus in the community.

BACKGROUND: Systemic lupus erythematosus (SLE) produces a wide range of symptoms, some of them mild; therefore it may be underdiagnosed. In a pilot study we tested the ability of a screening questionnaire to identify undiagnosed cases in the community. METHODS: A 10-item questionnaire was mailed to 3500 women aged 18-65 randomly selected from a general practice list in Birmingham, UK. A random sample of 300 non-respondents were sent two further mailings. Women returning the questionnaire with three positive answers were to attend for an antinuclear antibody (ANA) test; and those testing positive were to be referred to a rheumatologist for standard clinical assessment. FINDINGS: 1153 (30%) of the women responded, and 307 of these gave three or more positive answers on the questionnaire. The survey disclosed three women with previously undiagnosed SLE; and, in addition, it picked up all four of the women whose SLE had been diagnosed previously. INTERPRETATION: The prevalence of SLE revealed by this survey in Birmingham women is 200/100,000 (95% confidence interval 80 to 412), whereas the prevalence of diagnosed SLE in this age group is 54/100,000 (95% CI 47-62). Thus, a substantial number of undiagnosed cases exist, and further work needs to focus on the prevalence in different ethnic groups and the benefits of early diagnosis and treatment.

Adolescent↗
PubMed2002

Antiendothelial cell antibodies in systemic lupus erythematosus.

Sera from patients with systemic lupus erythematosus have been reported to contain IgM and/or IgG binding to endothelial cells (EC), i.e. anti-EC antibodies (AECA). Similar autoantibodies have been claimed to occur in a number of conditions associated with vasculitis. The original cyto-enzyme-linked immunosorbent assay (ELISA) remains the most widely used method for the detection of AECAs, although numerous pitfalls have been identified since then. These difficulties may explain why a consensus on the prevalence of AECAs has not been reached thus far. It is therefore desirable to confirm a positive result in the cyto-ELISA using other methods, such as flow cytometry, immunoprecipitation or Western blot. Yet, these methods appear to be difficult to use on a routine basis. With regard to the AECA effects, their binding induces activation of ECs, as substantiated by up-regulation of adhesion molecules, and synthesis of cytokines and chemokines, followed by their secretion. Some of these autoantibodies encourage the local production of tissue factor, and thereby favour coagulation. Other AECAs trigger apoptosis of ECs, although the Fas receptor does not seem to be involved in this process. In fact, since the target antigens are not well defined, the current challenge is to identify EC target molecules, and thus to gain further insights into the pathogenesis of diseases with vasculitis.

Autoantibodies↗
PubMed1986

Optic neuritis and myelopathy in systemic lupus erythematosus.

The optic neuritis of systemic lupus erythematosus (S.L.E.) more frequently results in the persistence of a central scotoma or complete blindness after a single attack than demyelinating optic neuritis, although the initial clinical presentations may be identical. A significant number of patients, however, recover normal vision. Optic neuritis may be the presenting symptom of S.L.E. and as myelopathy may also occur in the course of the disease, confusion with multiple sclerosis may result, especially if there are no arthritic, cutaneous nor visceral manifestations. We report a case of lupus optic neuritis associated with anticardiolipin antibodies and a circulating lupus anticoagulant and suggest these may be a marker for vasculitic optic neuritis and play a role in its aetiology.

Antibodies↗
PubMed2005

Fine mapping chromosome 16q12 in a collection of 231 systemic lupus erythematosus sibpair and multiplex families.

Systemic lupus erythematosus (SLE) is a chronic, autoimmune disorder influenced by multiple genetic and environmental factors. Linkage of SLE to chromosome 16q12-13 (LOD score=3.85) was first identified in pedigrees collected at the University of Minnesota, and has been replicated in several independent SLE collections. We performed fine mapping using microsatellites to further refine the susceptibility region(s), and the best evidence for linkage was identified at marker D16S3396 (LOD=2.28, P=0.0006). Evidence of association was suggested in the analysis of all families (D16S3094, P=0.0516) and improved to the level of significance (P=0.0106) when only the Caucasian families were analyzed. Subsets of pedigrees were then selected on the basis of clinical manifestations, and these subsets showed evidence for association with several markers: GATA143D05 (renal, P=0.0064), D16S3035 (renal, P=0.0418), D16S3117 (renal, P=0.0366), D16S3071 (malar rash, P=0.03638; neuropsychiatric, P=0.0349; oral ulcers, P=0.0459), D16S3094 (hematologic, P=0.0226), and D16S3089 (arthritis, P=0.0141). Together, these data provide further evidence that an important susceptibility gene(s) for SLE is located at 16q12.

Chromosomes, Human, Pair 16↗
PubMedDate not supplied

Cytokine polymorphisms in systemic lupus erythematosus and Sjögren's syndrome.

Systemic lupus erythematosus (SLE) and Sjögren's syndrome (SS) are defined genetically as complex diseases where multiple genes are involved in their pathogenesis. Among the genes of interest are those coding for the cytokines, molecules involved in immunoregulation that have been shown to play important roles in these diseases. Whether abnormalities in cytokine production are owing to genetic polymorphisms within the genes themselves is a matter of intensive study. The finding of functional polymorphisms within cytokine genes and their potential association with disease will open new avenues in their treatment.

Animals↗
PubMed2002

How does one assess and monitor patients with systemic lupus erythematosus in daily clinical practice?

Systemic lupus erythematosus (SLE) is a multisystem autoimmune rheumatic disease (ARD) characterized by flares and remissions. SLE has protean and often complex manifestations, necessitating careful clinical assessment. However, it is important to remember that not all clinical problems reported by a lupus patient are due to the disease. Some may be a consequence of therapy and others may be unrelated to lupus. Therefore it is important to understand the totality of the effect of the disease on the patient. In order to do this measures are needed which distinguish current, potentially reversible disease activity, permanent organ damage and the effect of the disease on the patients' health status. Several measures are in current use in clinical trials, but not all are suitable for use in the routine clinical setting. This chapter discusses the current measures available to assess disease activity and damage in SLE.

Health Status↗
PubMed2006

Involvement of a tissue-specific autoantibody in skin disorders of murine systemic lupus erythematosus and autoinflammatory diseases.

Human systemic lupus erythematosus (SLE) and its murine model, MRL lpr/lpr mice, are well known to develop a wide range of symptoms, such as glomerulonephritis, dermatitis, and arthritis, as an immune-complex disease. However, the deposition of circulating immune complex does not fully explain the tissue specificity of disease. Tissue-specific autoantigens may also be involved in tissue inflammation. In this study, desmoglein 3 (Dsg3), a major component of epidermal desmosomes, was identified as a skin-specific autoantigen. Several murine models of skin inflammation were found to develop autoantibodies to Dsg3 tightly correlated with disease aggravation, especially in MRL lpr/lpr mice. Furthermore, SLE-prone skin disease-free FcgammaRIIb-deficient mice developed skin inflammation upon immunization with Dsg3. Taken together with histological studies, we concluded that skin-specific Dsg3 serves as an autoantigen in chronic skin inflammatory diseases accompanied by mast cell degranulation, including both murine SLE and other autoinflammatory diseases.

Animals↗
PubMed1981

Mechanism of photosensitivity in systemic lupus erythematosus patients.

Patients who have systemic lupus erythematosus have increased numbers of chromosome breaks and rearrangements correlated with a low molecular weight chromosome-damaging agent that is released from their lymphocytes into the serum. This clastogenic factor also produces chromosome breaks and sister chromatid exchanges in healthy persons' lymphocytes when they are incubated in the presence of lupus patients' serum or lymphocytes or purified factor. The lymphocytes from lupus patients are sensitive to near-UV (360- to 400-nm light. This sensitivity seems to be related to the presence of the clastogenic factor in these cells; lymphocytes of healthy persons exposed to the factor also become sensitive to light of the same wavelengths. A significant increase in nonviable cells (trypan blue exclusion test) was observed after 5 min of irradiation with 360- and 380-nm light in the presence of the factor. The number of chromosome aberrations observed after stimulation of the irradiated lymphocytes with phytohemagglutinin was also maximal after irradiation at 380 nm in presence of the factor. The combined action of near-UV light plus clastogenic factor was inhibited by superoxide dismutase if the enzyme were present during irradiation, suggesting that activation involves photoproduction of superoxide ions. Irradiation of the purified factor and immediate addition of it to lymphocytes gave the same results whereas preirradiation of cells or of medium was without effect. The presence of this photoactivated agent explains why patients who have lupus erythematosus show an aggravated condition after exposure to sunlight and the appearance of typical skin lesions.

Cell Survival↗
PubMed1988

Presence of antibodies to ubiquitin during the autoimmune response associated with systemic lupus erythematosus.

Sera from patients with systemic lupus erythematosus (SLE) were shown to react with both ubiquitin and a synthetic fragment of it (residues 22-45) in an ELISA and with ubiquitin in immunoblotting experiments. Close to 80% of lupus patients possessed ubiquitin antibodies, whereas only 55% of them possessed native DNA antibodies, a marker of SLE. Less than 16% of patients with other rheumatic autoimmune diseases possessed antibodies to ubiquitin. Our results indicate that the combined measurement of antibodies to native DNA and to ubiquitin could appreciably increase the detection of SLE cases (up to 85% in our study). It is suggested that ubiquitin, a heat shock protein, could be involved in antibody formation against ubiquitin-protein conjugates present during cellular injury and that this represents a major characteristic of the autoimmune response in SLE.

Antibodies, Antinuclear↗
PubMed1998

A genome-wide search for susceptibility genes in human systemic lupus erythematosus sib-pair families.

Systemic lupus erythematosus (SLE) is an autoimmune multisystem inflammatory disease characterized by the production of pathogenic autoantibodies. Previous genetic studies have suggested associations with HLA Class II alleles, complement gene deficiencies, and Fc receptor polymorphisms; however, it is likely that other genes contribute to SLE susceptibility and pathogenesis. Here, we report the results of a genome-wide microsatellite marker screen in 105 SLE sib-pair families. By using multipoint nonparametric methods, the strongest evidence for linkage was found near the HLA locus (6p11-p21) [D6S257, logarithm of odds (lod) = 3.90, P = 0.000011] and at three additional regions: 16q13 (D16S415, lod = 3.64, P = 0.000022), 14q21-23 (D14S276, lod = 2.81, P = 0.00016), and 20p12 (D20S186, lod = 2.62, P = 0.00025). Another nine regions (1p36, 1p13, 1q42, 2p15, 2q21-33, 3cent-q11, 4q28, 11p15, and 15q26) were identified with lod scores >/=1.00. These data support the hypothesis that multiple genes, including one in the HLA region, influence susceptibility to human SLE.

Adult↗
PubMed1988

Autoantibodies to the constitutive 73-kD member of the hsp70 family of heat shock proteins in systemic lupus erythematosus.

Serum from patients with systemic lupus erythematosus (SLE) frequently contain IgM and IgG autoantibodies to the constitutively expressed 73-kD/pI 5.5 member of the hsp70 family of heat shock proteins, as determined by one-dimensional (SDS-PAGE) and two-dimensional (IEF/SDS-PAGE) immunoblotting, and by solid-phase SLE Ig immunoprecipitation experiments using hsp70 protein-specific mAbs as probes. Autoantibodies to hsp70 also were detected in a minority of sera from patients with other rheumatic or viral diseases, but not in normal sera. These data may provide additional insight into etiologic and pathophysiologic mechanisms in this and related autoimmune disorders.

Autoantibodies↗