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PubMed2007

Enhanced oxidative status but not corresponding elevated antioxidative status by anticardiolipin antibody and disease activity in patients with systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is associated with premature atherosclerosis, and an increased susceptibility of plasma lipids and lipoproteins to oxidation could at least in part promote atherogenesis. The objective of this study was to identify the effects of anticardiolipin antibody (aCL) and disease activity on oxidative and antioxidative status in patients with SLE. In this study, patients in SLE/aCL+ group and in SLE disease activity index >3 group had significantly higher thiobarbituric acid reactive substance (TBARS) levels, titers of autoantibodies against oxidized low-density lipoprotein (ox-LDL), and glutathione peroxidase activity than that of healthy controls. However, only TBARS and titers of autoantibodies against ox-LDL but not antioxidant enzyme activities were significantly different between SLE subgroups. Thus, enhanced oxidative status but not corresponding elevated antioxidative status by the presence of aCL and active disease activity make potent antioxidant therapy valuable for these SLE patients in preventing oxidative damage.

Adult↗

PubMed2005

Polymorphisms in the promoter region of RANTES in Han Chinese and their relationship with systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a complex multisystem autoimmune disease afflicting more than 600,000 individuals in China. RANTES (regulated on activation, normal T cell expressed and secreted, 17q11.2-q12) is a member of the proinflammatory cytokine family known as "chemokines". It plays an important role in the attraction and recruitment of lymphocytes, monocytes and eosinophils to sites of inflammation. A total of 146 SLE patients and 159 random healthy volunteer individuals in Han Chinese patients were enrolled in this study. Genotypes of RANTES -403 locus and -28 locus were observed to be different in all racial groups. The frequency of individuals who possessed G allele at -28 locus among SLE patients was not significantly different from that among normal controls. A total of seven compound genotypes at -403 locus and -28 locus were observed in this study. The frequency of this compound genotype (-403 G/G, -28 C/C) was different between the two groups. The distribution of genotypes and alleles at RANTES-403 locus was observed to be significantly different between renal damaged group and no renal damaged group (P<0.05), while there was no significant difference in distribution of genotypes and alleles at RANTES-28 locus between the two groups. These results suggest that (a) two genetic polymorphisms in the RANTES promoter do not correlate with SLE as individual polymorphisms. (b) interaction of the polymorphisms at two loci probably exerts a risk effect against SLE and (c) polymorphism at RANTES-403 locus is probably related with renal damage.

Alleles↗

PubMed2004

Chromosome 17p12-q11 harbors susceptibility loci for systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the presence of autoantibodies against intracellular components, the formation of immune complexes, and inflammation in various organs, typically the skin and kidney glomeruli. The etiology of the disease is not well understood but is most likely the result of the interaction between genetic and environmental factors. In order to identify susceptibility loci for SLE, we have performed genome scans with microsatellite markers covering the whole genome in families from Argentina, Italy, and Europe. The results reveal a heterogeneous disease with different susceptibility loci in different family sets. We have found significant linkage to chromosome 17p12-q11 in the Argentine set of families. The maximum LOD score was given by marker D17S1294 in combination with D17S1293, when assuming a dominant inheritance model (Z = 3.88). We also analyzed a repeat in the promoter region of the NOS2A gene, a strong candidate gene in the region, but no association was found. The locus on chromosome 17 has previously been identified in genetic studies of multiple sclerosis families. Several other interesting regions were found at 1p35, 1q31, 3q26, 5p15, 11q23 and 19q13, confirming previously identified loci for SLE or other autoimmune diseases.

Adult↗

PubMed2004

Association between IFNA genotype and the risk of systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is characterized by multisystem inflammation and production of autoantibodies, which can generate immune complexes and may cause tissue damage through the recognition of an autoantigen. Although many factors have been proposed, such as genetic factors, environmental factors, hormonal action, viruses, and dysregulation of cytokine production, the cause of this disease is not well understood. It has been reported that the levels of interferon (IFN)-alpha in the sera of some SLE patients are elevated and that IFN-alpha induces maturation of monocytes into highly active antigen-presenting dendritic cells (DCs). We analyzed the association between IFN-alpha genotype and the risk of SLE to clarify whether IFN-alpha plays a central role in susceptibility to SLE. The results showed that no IFN-alpha genotype was significantly associated with the risk of SLE.

Adolescent↗

PubMed2004

Trace elements and some extracellular antioxidant proteins levels in serum of patients with systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a chronic progressive autoimmune disorder with a wide spectrum of clinical and immunological abnormalities. In this study, we aimed to investigate the levels of serum zinc (Zn), copper (Cu), magnesium (Mg), manganese (Mn), iron (Fe), ceruloplasmin (Cp), transferrin (Trf), and albumin (Alb) in SLE and whether it is related to the severity of the clinical condition of this chronic disease. Cp and Cu levels were higher, while Trf, Alb, Zn, Mg, Mn, and Fe levels were lower in serum of patients with SLE (n = 27) compared with healthy controls (n = 20). The mechanisms by which these alterations occur in certain inflammatory conditions need to be elucidated. It is also obscure whether these alterations are a cause or a consequence of the inflammation. As a conclusion, alterations in the levels of the parameters in SLE may not be a reason for, but in fact a consequence of the disease itself.

Adolescent↗

PubMed2006

A positive correlation between homocysteine and brachial-ankle pulse wave velocity in patients with systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is associated with premature atherothrombotic complications. Hyperhomocysteinemia is considered a cardiovascular risk factor. Increased vascular stiffness may increase cardiovascular mortality. Pulse wave velocity (PWV) is a noninvasive method of analyzing vascular stiffness in the assessment of atherosclerosis. The objective of this study was to identify the relationship between plasma homocysteine levels and brachial-ankle pulse wave velocity (baPWV) measurement in SLE. Plasma homocysteine, baPWV, ankle-brachial index, blood pressure, C3, C4, anticardiolipin antibody (aCL), and anti-double-stranded DNA antibodies were determined in a total of 58 female patients with SLE. The control group comprised 32 age-matched healthy females. In addition, all patients were further classified into subgroups according to the presence of aCL (SLE/aCL+, n=27 vs SLE/aCL-, n=31) to determine the effect of aCL on the tested variables. The mean values for plasma homocysteine and baPWV were 13.19 mumol/l and 1,482 cm/s, respectively. Plasma homocysteine levels were significantly elevated in SLE patients when compared with the healthy controls. SLE patients with aCL had a significantly higher plasma homocysteine level than those without aCL. A significant positive correlation between plasma homocysteine and baPWV was found in patients with SLE (r=0.335, P=0.028, n=58). Plasma homocysteine also significantly correlated with right baPWV in all SLE patients (r=0.371, P=0.014, n=58) and in the SLE/aCL+ group (r=0.523, P=0.031, n=27). These findings indicate a possible link between plasma homocysteine and baPWV in SLE. In conclusion, SLE patients had an increased level of plasma homocysteine, and this phenomenon appeared to be related to vascular stiffness.

Adult↗

PubMed2002

An update on genetic studies of systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a complex, multifactorial autoimmune disease. Genetic factors are thought to contribute to its pathogenesis. There have been numerous recent advances in the study of murine and human lupus genetics. In well-defined experimental transgenic or gene-knockout mouse models, the development of lupus-like disease has implicated specific genes and pathways in the disease pathogenesis. Linkage analyses have mapped multiple susceptibility loci and disease suppressive loci using inbred strains of mice that spontaneously develop lupus-like disease. Elegant genetic dissection and function studies have led to the recent identification of two murine candidate susceptibility genes, Ifi202 (encoding an interferon-inducible protein) and Cr2 (encoding complement receptors 1 and 2). In human lupus, case- control studies have established associations of SLE with certain major histocompatibility class II alleles, complement deficiencies, and polymorphisms of Fc gamma receptor genes, a complement-related gene, and cytokine genes. During the past several years, linkage analyses using SLE multiplex families have provided many chromosomal regions for further exploration of susceptibility genes. Six regions exhibiting significant linkage to SLE are promising. Studies are underway to fine map these linked regions and to identify the genes in the susceptibility regions. An understanding of the genes involved in the development of lupus should provide targets for more focused therapy in lupus.

Alleles↗

PubMed2003

B lymphocytes and systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterized by B cell hyperactivity in association with autoantibodies, most prominently those directed to components of the cell nucleus. The source of the antigens that drive B cell responses in SLE is unknown, although recent studies suggest mechanisms by which the self-antigens become immunogenic and stimulate responses. Among these mechanisms, abnormalities in the generation of apoptotic cells or their clearance may increase the availability of nuclear antigens to drive responses. In addition, autoantibody crossreactivity may promote induction of responses to disparate antigens, foreign and self, and enable a single autoantibody to cause disease by crossreactive binding. In addition to reflecting increased exposure to self-antigen, autoantibody responses in SLE may result from abnormalities in B cell signaling and regulation by cytokines. New approaches to therapy aim to abrogate autoantibody production by targeting specific steps in B cell activation, including blockade of T cell costimulation.

Antibodies, Antinuclear↗

PubMed2000

Genetics and systemic lupus erythematosus.

Systemic lupus erythematosus is a complex, multifactorial, autoimmune disease. Genetic factors are believed to contribute to its pathogenesis. There have been numerous recent advances in the study of both murine and human lupus genetics. In murine lupus, congenic strains of three susceptibility loci have been developed. Transgenic and knock-out mice models of candidate genes now exist. In association studies of human lupus, the contributions of the MHC loci, Fcgamma receptors, various cytokines, components of the complement cascade, and proteins involved in apoptosis have been explored. Most recently, linkage analyses have been performed and provide numerous regions for further exploration for susceptibility genes. Studies to identify the genes in the susceptibility regions are underway. An understanding of the genes involved in the development of lupus should provide targets for more focused therapy.

Animals↗

PubMed1993

Chronic pancreatitis: a complication of systemic lupus erythematosus.

Systemic lupus erythematosus (SLE), an autoimmune disease with multisystem involvement, has been reported to be associated with a number of gastrointestinal complications. Acute pancreatitis is an unusual manifestation of this disorder. This report presents two cases of patients with SLE who developed chronic pancreatitis with no other identifiable etiology.

Adult↗

PubMed1985

Interleukin-2 restores the depressed allogeneic cell-mediated lympholysis and natural killer cell activity in patients with systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is characterized by a variety of profound T-cell abnormalities among which are decreased cytotoxic capacity measured by allogeneic cell-mediated lympholysis (CML), natural killer cell (NK) activity, and decreased lymphokine production. In a group of 13 patients with active SLE, allogeneic CML, tested by a 4-hr 51Cr-release assay, was 18.2 +/- 2.7% while in the group of normal individuals CML was 41.2 +/- 2.7%. If optimal doses of affinity-purified interleukin-2 (IL-2) were present during the mixed lymphocyte culture, the CML of SLE patients was increased to normal levels (40.4 +/- 4.0%). In contrast, interferon-alpha (IFN-alpha) increased (but not significantly) the levels of CML. Mixed lymphocyte reaction, tested by tritiated thymidine incorporation, was also decreased in the group of patients (14,820 +/- 815 cpm vs 28,972 +/- 5880 cpm in normals) and it was increased to normal levels if IL-2, but not IFN-alpha was added to the cultures. NK activity was decreased in the group of patients tested by 51Cr-release assay, harvested at 6 and 18 hr. IL-2 increased the NK activity up to normal levels, while IFN-alpha was only partially efficacious. These results demonstrate that IL-2, but not IFN-alpha, can potentiate or even fully restore the deficient cytotoxic effector function of peripheral mononuclear cells in patients with SLE.

Cytotoxicity, Immunologic↗

PubMed1989

Monocyte function in systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is characterized by multiple defects affecting B and T lymphocyte cell function. In view of the influence that monocytes may have on these functions, we have examined monocyte function in patients with SLE and normals. Monocytes were examined as to number, their ability to modulate IgG synthesis, phagocytose yeast particles, and acid phosphatase activity. Patients had more monocytes and mononuclear cells made more IgG, but these factors appear to be independent of each other. Monocytes from lupus patients are less phagocytic but show similar levels of acid phosphatase activity to normal controls. Normal, but not lupus monocytes, show enhanced phagocytosis following treatment with LPS. The effect of monocyte stimulation on acid phosphatase activity is the same in lupus and normal monocytes. Taken together, these observations suggest that the increased numbers of monocytes in lupus patients and some subtle functional differences in these cells may be important in the progression of this disease.

Humans↗

PubMed1992

Autoantibodies in pet dogs owned by patients with systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) occurs in human beings and in dogs. There is evidence to suggest that the disease is caused by a transmissible factor that may cross the species barrier. We investigated this possibility by looking for autoantibodies and serum protein abnormalities in serum samples from 15 pet dogs owned by patients with SLE and comparing results with those obtained with serum from 10 healthy dogs kept in a controlled environment and 9 dogs with autoimmune diseases. We used standard immunological assays modified for use with canine samples. Compared with the normal dogs, increased amounts of antibody to double-stranded DNA were found in serum from the SLE patients' dogs (median optical density [405 nm] = 0.117 vs 0.299; p = 0.0001), this latter amount being similar to that found in serum from the autoimmune group (0.201; p = 0.6). Abnormal serum protein electrophoresis patterns were found in samples from the autoimmune and SLE patients' dogs but not the normal dogs. These findings support the idea that exposure to common environmental factors or transmissible agents may have a role in causing SLE.

Animals↗

PubMed1992

Primary total hip arthroplasty in systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a chronic inflammatory disease affecting primarily young women. Osteonecrosis of the femoral head produces significant morbidity in these patients. The clinical and radiographic results of 33 total hip arthroplasties (THA) in 25 patients were studied. The Hospital for Special Surgery hip rating was good or excellent in all surviving index primary hip arthroplasties at a median follow-up of 47 months. Overall survival probability was 94.6% at 5 years and 81.8% at 9 years using survivorship analysis. Perioperative morbidity was minimal. Total hip arthroplasty using contemporary techniques and current management protocols can provide reliable functional improvement in patients with osteonecrosis secondary to SLE.

Adult↗

PubMed1989

1,25 dihydroxyvitamin-D3 regulation of immunoglobulin production in peripheral blood mononuclear cells of patients with systemic lupus erythematosus.

Systemic Lupus Erythematosus (SLE) is a multisystem disease characterized by an increase in the secretion of autoantibodies. The mechanisms of autoantibody-induced disease have not been clarified. 1,25-Dihydroxy-vitamin D3 (1,25-D3) is known to be important in the regulation of normal human lymphocyte functions. Among its regulatory functions is the ability to inhibit mitogen-stimulated production of immunoglobulin. The experiments reported here explored the regulation of IgG production by peripheral blood mononuclear cells (PBMCs) of patients with inactive and active SLE. 1,25-Dihydroxyvitamin D3 inhibited mitogen-stimulated IgG production in cells from normal individuals and inactive SLE patients, but not spontaneous IgG production by PBMCs from active SLE patients. Addition of exogenous IL-2 (5-50 U/ml) to 1,25-D3-treated cells from all patient groups did not affect IgG production significantly under any conditions tested. The addition of IL-2 to PMBCs had no effect on IgG production in normal individuals or inactive SLE patients, but stimulated IgG production in PBMCs of active SLE patients. We conclude that the regulation of mitogen-stimulated IgG production in inactive SLE patients by 1,25-D3 and IL-2 is similar to normal individuals, but IgG production by active SLE PBMCs is unresponsive to 1,25-D3 regulation and is increased with the addition of IL-2.

Adult↗

PubMed2005

Immunotherapy of systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a remarkably heterogeneous multisystem autoimmune disease. Improved understanding of the immunopathogenesis of this disorder over the past two decades is now being applied to therapy, with treatment being directed at specific immunological targets. This review will focus on both new uses for established therapies as well as on the introduction of novel agents. It is premature to claim that any one agent has superior efficacy to current therapies. However, the willingness of investigators supported by the pharmaceutical and biotechnology industries to evaluate the efficacy and safety of new products in controlled clinical trials may provide answers.

Humans↗

PubMed2004

Stem cell transplantation in systemic lupus erythematosus.

Systemic lupus erythematosus is a heterogeneous, multisystem disease responsive to treatment with corticosteroids and immune suppressives. Many patients fail to achieve treatment-free remissions, and their long-term outcomes remain poor owing to the development of vital organ failure, cumulative drug toxicity and an increased risk of cardiovascular disease and malignancy. Haematopoietic stem cell transplantation (HSCT) offers the potential to improve long-term outcome in those with a poor prognosis. Preliminary phase II and registry studies have usually employed non-myeloablative conditioning with positive CD34 cell selection. They have highlighted the potential efficacy and dangers of HSCT. Patient selection is important but complex, and the influence of HSCT on long-term outcome is unknown. Disease relapse occurs in up to one-third of patients after HSCT, but the consequences of relapse and the role of remission-maintenance strategies are unknown. With the availability of other alternative therapies in refractory disease, there needs to be a clear demonstration of the benefits of HSCT from current randomized trials.

Bone Marrow↗

PubMed2006

The role of nitric oxide in abnormal T cell signal transduction in systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by production of antinuclear autoantibodies and diverse array of clinical manifestations. T cells from patients with SLE have been shown to be activated in vivo and provide help to autoreactive B cells. Lupus T cells exhibit enhanced spontaneous and diminished activation-induced apoptosis and predisposition to necrosis. Persistent mitochondrial hyperpolarization and ATP depletion - associated with significantly increased mitochondrial mass - characterize T lymphocyte dysfunction in SLE. In addition to cell death abnormalities, mitochondrial dysfunction is associated with altered signal transduction through the T cell receptor and Ca2+ fluxing. Exposure of normal T cell to nitric oxide induces mitochondrial hyperpolarization and biogenesis and regenerates the Ca2+ signaling profile of lupus T cells. This article reviews a novel understanding of the role of nitric oxide in signal transduction and cell death abnormalities in SLE.

Animals↗