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PubMed1995

Significance of antibodies to cardiolipin in unselected patients with systemic lupus erythematosus: clinical and laboratory associations. The SLE Study Group.

In a multicentre study anticardiolipin antibodies of the IgG and IgM isotypes were measured by a solid phase enzyme immunoassay in 368 patients with systemic lupus erythematosus (SLE) who were not selected on the basis of features of antiphospholipid syndrome. Clinical and laboratory associations of increased levels of anticardiolipin antibodies were evaluated. IgG and IgM antibodies to cardiolipin were documented in 224 (60.9%) and 128 (34.8%) patients, respectively. Regarding the symptoms of antiphospholipid syndrome, elevated amounts of anticardiolipin IgG were significantly associated with spontaneous abortion (P < 0.001), thrombocytopenia (P < 0.01), livedo reticularis (P < 0.01) and a positive direct Coombs test (P < 0.05), but not with thrombosis or central nervous system diseases such as epilepsy and psychosis. IgM antibodies to cardiolipin were associated with a positive direct Coombs test (P < 0.01), but with no other symptom of antiphospholipid syndrome. The predictive values of anticardiolipin antibody determinations in unselected SLE patients were poor for all features of antiphospholipid syndrome because of high proportions of false-positive and false-negative results. As for other manifestations of SLE, positive correlations between raised antibodies to double-stranded DNA and the occurrence of anticardiolipin antibodies of the IgG isotype were observed, and anticardiolipin IgM was negatively associated with nephritis.

Adolescent↗

PubMed1994

HLA class II genes and antibodies against recombinant U1-nRNP proteins in patients with systemic lupus erythematosus. SLE Study Group.

To investigate a possible involvement of HLA-class II alleles in the genetic predisposition for the formation of anti-U1-nRNP antibody-in systemic lupus erythematosus (SLE), genomic DNA of 178 patients was typed for the DRB1, DQA1 and DQB1 alleles using a polymerase chain reaction (PCR) and non-radioactive-oligonucleotide typing. Antibodies against recombinant U1-nRNP proteins (U1-A-, U1-C- and 70K-protein) were determined by ELISA. Anti-U1-C antibody was found in 26 (14.7%), anti-U1-A in 34 (19.2%) and anti-70K in 17 (9.6%) patients. A joint occurrence was observed for these antibodies against the recombinant U1-nRNP proteins: anti-U1-C and anti-U1-A antibodies occurred together more frequently than alone and than together with anti-U1-70K antibodies. The frequency of DRB1*04 was slightly increased in the patients with anti-U1-C as compared to the patients without anti-U1-C (P < 0.05, Pcorr = n.s., RR = 2.4). The DQA1*0301 allele, which is in linkage disequilibrium with DRB1*04, is found more frequently in anti-U1-C-positive than in antibody-negative patients. The DQB1*0303 allele, detected in 12 of 176 SLE patients, was absent in the patients with any of the antibodies against the U1-nRNP proteins. All these deviations may be due to chance alone. We concluded that the presence of antibodies against recombinant U1-nRNP proteins was not significantly associated with any HLA DRB1, DQA1 and DQB1 allele in our group of SLE patients.

Alleles↗

PubMed1995

Characterization of B-cell lines from SLE patients and their relatives.

Epstein-Barr-virus (EBV)-transformed lymphoblastoid B-cell lines were generated from peripheral blood lymphocytes of 55 patients with systemic lupus erythematosus (SLE) and 44 healthy relatives. All donors have previously been extensively characterized with regard to clinical, serologic, and genetic parameters. Here, peripheral blood lymphocytes and lines were characterized for cell surface antigens. Furthermore, autoantibody production and proliferation rate of the cell lines were monitored. A significant difference between patients and relatives was the lower proliferation rate of EBV-transformed cell lines of the SLE patients. All SLE cell lines are available for interested researches and can be obtained from the European Cell Bank, Salisbury, UK.

Antigens, Surface↗

PubMed1995

Autoreactivity to mouse C1q in a murine model of SLE.

A large proportion of systemic lupus erythematosus (SLE) patients develop glomerulonephritis, coincident with the appearance of autoantibodies to C1q, the Fc-recognizing collagen-like subcomponent of the first component of complement, C1. The MRL/lpr/lpr mouse is an established model for SLE, developing both antinuclear and anti-type II collagen autoantibodies, and rheumatoid factors(s), exhibiting reduced complement levels and later on developing glomerulonephritis and often arthritis. We report here an age-dependent decrease in serum C1q levels coincident with the development of IgG2b autoantibodies reactive with mouse C1q in MRL/lpr/lpr mice. Unlike IgG2b, although high levels of IgM, IgG1 and IgG2a are present in these mice, few, if any, antibodies of these subclasses reactive with mouse C1q were observed in this study. This is the first report of autoantibodies against autologous C1q in an animal model, and the results should facilitate in clarification of the roles of C1q and autoantibodies reactive with C1q in SLE, as well as their potential connection with glomerulonephritis.

Animals↗

PubMed1991

Immunoglobulin allotypes are not associated with HLA-antigens, autoantibodies and clinical symptoms in systemic lupus erythematosus. Members of the SLE Study Group.

Immunoglobulin heavy chain (G1m, G2m, G3m, A2m) and kappa light chain (Km) allotype and phenotype frequencies of 323 central European Caucasian patients with systemic lupus erythematosus (SLE) were examined and correlated with various genetic, serologic and clinical markers of SLE. No significant associations were found between immunoglobulin allotypes or phenotypes and all 20 parameters tested (nephritis, vasculitis, arthralgias, photosensitivity, discoid lesions, central nervous system disease, Raynaud's phenomenon, sex, anti-Ro, anti-La, anti-nRNP, HLA-DR1-DR7, HLA phenotypes B8-DR3, B7-DR2). It could therefore be assumed that Gm, A2m and Km allotypes were not associated with HLA-antigens and had no influence on the serologic and clinical expression of SLE.

Autoantibodies↗

PubMed1996

Clinical and immunological aspects of autoantibodies to RA33/hnRNP-A/B proteins--a link between RA, SLE and MCTD.

Heterogeneous nuclear ribonucleoprotein (hnRNP) complexes are major constituents of the spliceosome. They are composed of approximately 30 different proteins which can bind to nascent pre-mRNA. Among these, the hnRNP-A/B proteins form a subgroup of highly related proteins consisting of two adjacent RNA binding domains (RBD) within the N-terminal parts, whereas the C-terminal halves contain almost 50% glycine residues. These proteins, in particular A2/RA33, are targeted by autoantibodies from patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and mixed connective tissue disease (MCTD). In SLE anti-hnRNP antibodies frequently occur together with antibodies to U1 small nuclear RNP (U1-snRNP) and Sm, other proteins of the spliceosome. Preliminary epitope mapping studies have revealed major antibody binding sites in the RNA binding regions for all three diseases. Nevertheless, there is some indication of disease specific epitope recognition. Studies in animal models have demonstrated anti-RA33/hnRNP-A/B antibodies in lupus-prone mouse strains. Thus, autoantibodies to the spliceosomal hnRNP-A/B proteins are a common feature of RA, SLE, and MCTD. However, these diseases differ in their reactivities to other spliceosomal proteins, especially anti-U1 snRNP and Sm. Therefore, anti-RA33/hnRNP-A/B autoantibodies are not only valuable diagnostic markers but may also allow additional insights into the pathogenesis of rheumatic autoimmune diseases.

Animals↗

PubMed1985

Alteration of Fc-receptor phenotype and proliferative capacity of Fc-IgG-receptor positive lymphocytes through interaction with soluble immune complexes of patients with SLE or RA.

Soluble circulating immune complexes (CIC) are a common finding in patients with systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) or other autoimmune diseases. The predominant immunoglobulin class of most CIC is IgG, which enables these CIC to bind to Fc-IgG-receptor expressing cells. In this study the interaction between soluble CIC from patients with SLE or RA and Fc-IgG-receptor positive lymphoid cells from healthy individuals was investigated. Similar to the effect observed with insoluble immune complexes, soluble CIC interact with Fc-IgG-receptor positive lymphoid cells and can induce a modulation of Fc-receptor expression. Fc-IgG-receptors are lost and Fc-IgM-receptors are expressed on the same cells after IC interaction and culturing the cells for 24 h. Simultaneously with this change of Fc-receptor phenotype the originally Fc-IgG-receptor positive cells demonstrate a decreased ability to proliferate upon mitogen stimulation. This change of phenotype and proliferative capacity correlates with the content of CIC in the sera of patients with SLE or RA.

Antigen-Antibody Complex↗

PubMed1994

T helper cell dysfunction in systemic lupus erythematosus (SLE): relation to disease activity.

Patients with systemic lupus erythematosus (SLE) are known to have defects in both humoral and cellular immunity. The significance of defective T cell-mediated immunity and its relationship to disease activity have not been clearly established. We studied in vitro T helper cell (Th) function in 150 SLE outpatients and correlated Th function with validated measures of disease activity. Interleukin 2 (IL-2) production by peripheral blood mononuclear cells (PBMC) was measured after stimulation with the recall antigens influenza A virus (FLU) and tetanus toxoid (TET), irradiated allogeneic peripheral blood mononuclear cells (ALLO), and phytohemagglutinin (PHA). We observed three patterns of Th response: (1) 76 of 150 (50%) of patients responded to the recall antigens FLU and/or TET, ALLO, and PHA; (2) 62 of 150 (42%) of patients did not respond to recall antigens but responded to ALLO and PHA; and (3) 12 of 150 (8%) of patients did not respond to either recall antigens or ALLO antigens. This diminished T cell function was correlated with higher disease activity as measured by four scales of clinical activity, such that individuals who exhibited more in vitro immune dysfunction presented with significant increases in their clinical activity indices. The alterations in T cell function could not be accounted for by medication doses alone. Thus, SLE patients have multiple distinct defects at the level of the Th cell which are associated with clinical measures of disease activity.

Adult↗

PubMed1995

Modulation of the immunoglobulin dysregulation in GvH- and SLE-like diseases by the murine IL-4 receptor (IL-4-R).

As has been reported previously, models of chronic graft-versus-host (GvH) and systemic lupus erythematosus (SLE)-like diseases are characterized by high IgE and IgG1 immunoglobulin (Ig) levels in the serum. An IL-4 induced pathological expansion of Th2 helper cells has been described for both disease models. Due to the immunopharmacological profile of soluble recombinant interleukin-4 receptor (IL-4-R) to bind specifically the corresponding ligand IL-4 and thereby to modulate biological activity upon exogenous administration in various autoimmune disease models, we investigated the immunoregulatory activity of IL-4-R and anti-IL-4 monoclonal antibody (MAb) 11B11 on the development of SLE-like disease in MRL/lpr autoimmune mice and on chronic GvH reaction in BDF1 hybrid mice. Sensitized GvH-BDF1 hybrid mice and SLE in MRL/lpr autoimmune mice were treated in vivo with the IL-4 antagonists to alter the pattern of serum Ig production and to modulate the disease process. These animals were followed for proteinuria, autoantibody production (anti-dsDNA), serum IgE, IgG1 and IgG2a levels, and the survival was monitored. Treatment of these diseased animals resulted in an improved survival rate, lowered the percentage of animals with lymphadenopathy and hepatosplenomegaly, reduced the levels of autoantibodies and inhibited proteinuria of the developing glomerulonephritis in both mouse strains, even in the established diseases. In both models the increase in total IgE and IgG1 levels in serum was strongly inhibited by the IL-4 antagonists, even under therapeutic conditions. But there was no inhibitory activity observed on the IgG2a serum levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

The use of the murine chronic graft vs host (CGVH) disease, a model for systemic lupus erythematosus (SLE), for drug discovery.

Studies were conducted to evaluate the use of a murine SLE-like disease for the discovery of novel drugs: This disease is the result of a chronic form of a graft vs host (GVH) reaction. Using prednisolone (Pr), cyclophosphamide (Cy), indomethacin (Indo), and the isoxazol derivative, HWA 486, we found that only Indo was ineffective in inhibiting the SLE symptoms. Interestingly, HWA 486, which did not display any immunosuppressive activity, restored the suppressed T-cell response to the same level as found in healthy mice. We feel that this murine model of SLE could be of value for discovering substances with novel antirheumatic, and/or immunomodulating activities.

Animals↗

PubMed1997

IL-10 production in multiple sclerosis patients, SLE patients and healthy controls: preliminary findings.

IL-10 is a cytokine with suppressive effects on (auto) antigen presentation and T-cell-mediated immune reactions, but is also capable of stimulating polyclonal IgG synthesis. Recent evidence suggests its involvement in multiple sclerosis (MS) and systemic lupus erythematosus (SLE). We assessed PBMNC IL-10 release in MS and SLE patients before and after in vivo prednisone or methylprednisolone treatment. The SLE patients showed a high level of IL-10 release by unstimulated PBMNCs, whereas the PHA-stimulated PBMNCs from MS patients produced large amounts of the cytokine.

Adult↗

PubMed1987

Articular mobility in systemic lupus erythematosus (SLE).

The study was prompted by the suggestion that inflammatory polyarthritis and corticosteroids increase articular mobility. Ninety female patients with systemic lupus erythematosus (SLE) of whom 85 had polyarthritis and at least 75 of whom had received corticosteroid therapy were studied and compared to an equal number of carefully matched controls. The difference between the number of hypermobile patients [6 (7%)] and controls [5 (6%)] was not significant. There was also no significant difference when either the pooled mobility scores or the pooled hand scores of the patients and controls were compared. No significant association between articular mobility and either age at onset of disease, duration of disease or corticosteroid therapy was demonstrated. There was a significant association between deformity and duration of disease (p = 0.04) but not with mobility score. We conclude that SLE patients do not have a hypermobile tendency and therefore that neither SLE nor corticosteroids predispose to increased articular mobility. There is also no association between articular mobility and deformity.

Adolescent↗

PubMed1994

Lymphocytotoxic antibodies in SLE: a review of the literature.

In a great majority of patients with systemic lupus erythematosus (SLE) lymphocytotoxic antibodies (LCA) are detected. The reported prevalence depends on the methods of detection and definition of test-positivity. The pathogenetic role of LCA remains unclear. Different reports show that LCA can have an influence on mononuclear cell function, e.g., on production of interferon, or specifically on T-cell function. In several studies T-cell specificity of LCA cannot be shown. Sometimes an overlap between LCA and anti-B2M antibodies is found, suggesting that LCA have anti-B2M activity. Anti-B2M activity might have an impact on T-cell as well as on B cell function. Next to the anti-B2M activity, binding to nuclear material is claimed. Investigating the role of LCA in respect to lymphopenia, a direct relationship cannot be found; however, LCA might induce interferon production, resulting in lymphopenia. Several studies show or claim a relationship between the presence of LCA and neurological manifestations in SLE patients; the results, however, remain questionable due to the difference in detection methods as well as in definition of central nervous system (CNS) involvement. In other studies, an increased incidence of LCA is reported in relatives of SLE patients as well. In addition, LCA are reported in quite a lot of other diseases such as rheumatoid arthritis, ankylosing spondylitis, malignancies and viral illnesses. This latter association has led to the assumption that LCA might have a virus-related origin.

Antilymphocyte Serum↗

PubMed1994

Autoimmune multiorgan involvement in elderly men is it SLE?

Systemic lupus erythematosus (SLE) in males and especially in the elderly is infrequent. We describe two male patients over 65 years old, who presented with anaemia, cytopenia, nephritis, and serositis, suggesting that they suffered from an autoimmune disease. Following an interval of 6 and 9 years respectively, the diagnosis of SLE was made. In both patients, hypothyroidism, and eye involvement (uveitis and iridocyclitis) were present indicating autoimmune activity or even a new autoimmune syndrome. One patient was treated with corticosteroids and azathioprine upon which he developed many side effects from the steroid therapy. The other patient received treatment with intravenous immunoglobulin (IVIG), and at a follow-up period of 18 months, the patient's condition remained stable. We suggest that in the constellation of clinically multiple organ involvement in the elderly male, the diagnosis of SLE should be considered. IVIG may be a successful alternative therapy in this subset of patients.

Aged↗

PubMed2000

Early and delayed Tc-99m ECD brain SPECT in SLE patients with CNS involvement.

We compared early and delayed Tc-99m ECD SPECT scans in 32 SLE patients (Group 1, definite neuropsychiatric disorders; Group 2, minor neurologic symptoms or normal) with those of normal controls by visual inspection and semi-quantitative evaluation. With visual interpretation, 13 out of 14 patients in Group 1 (93%) and 7 out of 18 patients in Group 2 (39%) had diffuse uneven decrease in early scans. Seven patients in Group 2 (39%) who had normal early scans demonstrated focal decrease in the medial frontal lobe in delayed scans. With cerebral region to cerebellar ratios, in early scans, the medial frontal lobe in Group 1 and Group 2 was significantly lower than in normal controls, and lateral frontal lobe and occipital lobes in Group 1 were significantly lower than in normal controls. Nevertheless, in delayed scans, every cortical region except for the parietal lobe in Groups 1 and 2 was significantly lower than in normal controls. The retention rates in all regions in SLE patients were significantly lower than in normal controls. No case showed SPECT improvement on follow-up studies in either group in spite of clinical improvement. Delayed Tc-99m ECD brain SPECT of high sensitivity might be useful in detecting CNS involvement. Although the SPECT findings did not correlate with the neuropsychiatric symptoms, early and delayed Tc-99m ECD SPECT seems to provide useful objective diagnostic information in SLE patients.

Adult↗

PubMed2001

Progression of primary APS (Hughes syndrome) into serological SLE: case report.

An Arab woman presented with a history of multiple foetal losses and spontaneous venous thromboembolism, which recurred on several occasions. The presence of antiphospholipid antibodies in the absence of other clinical and serological features of systemic lupus erythematosus (SLE), including negative antinuclear antibodies (ANA), confirmed the diagnosis of primary antiphospholipid syndrome (PAPS). More than 15 years after the beginning of clinical events and 10 years after diagnosis, she progressed into the immunological domain of SLE without concurrent clinical features. The patient exhibited weakly positive ANA of a speckled pattern, strongly positive anti (ds) DNA antibodies and false positive VDRL. Lymphopenia has not been observed at any stage of the follow-up. Although the evolution of PAPS into SLE has been infrequently reported, this seems to be another case suggesting that PAPS in some patients may be an early manifestation of lupus.

Adult↗

PubMed2006

Current topics in human SLE genetics.

Susceptibility to systemic lupus erythematosus (SLE) depends on genetic and environmental factors. Genome scan studies have identified eight chromosomal regions with significant linkage to SLE that are confirmed by individual cohorts, suggesting that susceptibility genes may be identified within each of these loci. Linkage studies and single nucleotide polymorphisms (SNPs) have led to the identification of positional candidate genes, and their functional allelic variants have demonstrated molecular pathogenesis of the disease. The discovery of positional candidate genes that are associated with various autoimmune diseases signifies a common pathway in the mechanism of these diseases. Copy polymorphisms in susceptibility genes provide evidence in how genetic plasticity affects complex phenotypes as seen in SLE.

Genetic Linkage↗

PubMed1997

A fatal case of severe SLE complicated by invasive aspergillosis.

We report on the case of a 25-year-old female with severe systemic lupus erythematosus (SLE) who presented with pancytopenia, fever, arthralgia and abdominal pain. After antibiotic treatment, the patient was afebrile for 3 days before her temperature rose again. Dyspnoea and cough pointed towards pneumonia which was confirmed by X-ray. Different antibiotics and the antimycotic agent fluconazol were given. The lupus flare was treated with high-dose prednisolone. After a couple of days, the dyspnoea increased and mechanical ventilation became necessary. Bronchoscopy and transbronchial biopsy revealed the diagnosis of invasive aspergilloses. Despite of an immediate treatment with amphotericin B, the patient died because of respiratory insufficiency. The literature on aspergillosis in SLE is reviewed and prophylactic, diagnostic and therapeutic options are discussed for this infectious complication which has an 80% mortality in patients with SLE.

Adult↗