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PubMedDate not supplied

Complement system studies in systemic lupus erythematosus (SLE)

Complement system involvement has been studied in 16 patients with systemic lupus erythematosus (SLE). Circulating conversion products of C3 were observed in 4 cases. Low mean values of C4 and C3 were found, while C3 proactivator (properdin factor B) levels were low in only a few of the patients. The levels of C4, C3 and C3 proactivator were not lower in the 4 patients in whom C3 conversion products could be demonstrated than in the others. It is concluded that the low complement values found in SLE may be caused mainly by deficient synthesis. Signs of complement activation are in this patient material demonstrated early in the disease, and chiefly in patients not receiving immunosuppressive therapy.

Adolescent↗

PubMed1996

Behçet's disease as a part of the symptom complex of SLE?

Systemic lupus erythematosus and Behçet's disease are known to be induced by immunoregulatory defects and to have some identical manifestations. Although the possibility of the coexistence of these disorders exists only one example of an association of these disorders has been described previously by Lee et al. Therefore, we describe an example of typical SLE with additional symptoms of Behçet's disease as a part of the symptom complex of SLE.

Adult↗

PubMed2005

Bullous Systemic Lupus Erythematosus as an Initial Manifestation of SLE.

Bullous systemic lupus erythematosus (BSLE) is a rare subset of systemic lupus erythematosus that is often associated with autoimmunity to type VII collagen. We describe a 45-year-old woman with BSLE who presented with vesiculobullous lesions as an initial manifestation of SLE. The patient first noticed a widespread urticarial, erythematous eruption associated with tense blisters, erosions, and crusting. She was diagnosed with bullous pemphigoid and underwent a one-month course of treatment with betamethazone. Because of the appearance of marked proteinuria, a subsequent renal biopsy, and serological tests, the patient was diagnosed with rapidly progressive glomerulonephritis and systemic lupus erythematosus. The patient's IgG circulating antibodies labeled the dermal floor of salt-split skin and recognized type VII collagen in immunoblot studies. Although methylprednisolone pulse therapy for glomerulonephritis did not alleviate the vesicullobullous eruption, treatment with dapsone resulted in dramatic disappearance of the lesions. Cessation of dapsone therapy due to hemolysis with Heinz-body formation did not aggravate the bullous disease. Our case illustrates that a generalized vesiculobullous eruption can be the sole presenting manifestation of SLE. It also emphasizes the close temporal relationship between BSLE and lupus nephritis.

Betamethasone↗

PubMed1992

T lymphocyte expression of complement receptor 2 (CR2/CD21): a role in adhesive cell-cell interactions and dysregulation in a patient with systemic lupus erythematosus (SLE).

Complement receptor 2 (CR2, CD21), the receptor for both the C3d,g portion of human complement component C3 and the Epstein-Barr virus, has been recently described on peripheral T cells. By using dual stain flow cytometric analysis, we have also observed that a peripheral T lymphocyte subpopulation of normal healthy donors bears CR2 in a range varying from 1.1 to 23.2% (mean 12.6%) of total CD3+ cells. T lymphocytes from nine patients with inactive SLE expressed CR2 in a similar range. Three patients with active SLE were also studied. One of them, having neuropathy and glomerulonephritis, displayed an expansion of the CR2 T cell subpopulation which reached as much as 89% of total CD3+ cells. To examine potential functional roles of T cell CR2, cells from a Jurkat-derived CR2 expressing T cell line were found to bind in vitro to human CR2-, complement-coated K562 cell targets in a CR2- and complement-dependent fashion. Based on these studies, we hypothesize that CR2 might act to increase adherence of T cells to nucleated target cells bearing C3d,g, a function which may be relevant to cytotoxicity or other T cell activities requiring cell-cell interaction.

B-Lymphocytes↗

PubMed1993

C1 inhibitor functional deficiency in systemic lupus erythematosus (SLE).

C1 inhibitor (C1-inh) was assayed in eight SLE patients presenting with consistently low levels of intact C4. C1-inh antigenic levels were normal in all patients; however, the function of the C1-inh tested against C1s and C1r was variable and outside the normal functional range in seven of the eight patients. The molecular weight of patients' C1-inh protein was 105 kD, corresponding to the size of the intact molecule. The C1-inh gene was analysed in all patients. Restriction fragments generated with TaqI, PstI and HgiAI gave no indication of a major C1-inh gene rearrangement. Direct genomic sequencing of exon VIII revealed three polymorphic point mutations, but there were no changes from the normal gene in or around the reactive-centre residue of C1-inh. Furthermore, we found no evidence for a C1-inh autoantibody in patients which could affect normal C1-inh function in vitro. These results indicate that the etiology of C1-inh dysfunction in SLE is heterogeneous and distinct from that reported in either hereditary or acquired angioedema.

Base Sequence↗

PubMed2004

The candidate gene approach: have murine models informed the study of human SLE?

Genome wide linkage studies in human SLE have identified seven highly significant loci linked to SLE, and more than 20 other loci showing suggestive linkage to disease. However, pin-pointing the susceptibility alleles in candidate genes within these linkage regions is challenging, due the genetic heterogeneity, racial differences and environmental influences on disease aetiology. Utilization of murine models of spontaneous lupus nephritis provide a complementary approach, which may then identify candidate genes for analysis in human cases. This review highlights the utility of cross-species approach to identify and characterize the effect of given candidate genes in lupus. The examples described in this review demonstrate the importance of bringing together both genetic and functional information in human and mouse studies.

Animals↗

PubMed1979

Studies of anti-lymphocyte antibody of patients with active SLE. I. Cause of loss of suppressor T-lymphocyte function.

Effect of anti-lymphocyte antibody of active systemic lupus erythematosus (SLE) on lymphocyte function was examined. Lymphocytes from normal individuals treated with anti-lymphocyte antibody and complement exhibited marked inhibition of response to concanavalin A (Con A), while the response of lymphocytes to phytohaemagglutinin M (PHA-M) and pokeweed mitogen (PWM) was slightly affected. In mixed lymphocyte culture response, both stimulator and responder cells were insensitive to anti-lymphocyte antibody. Treatment of sensitized lymphocytes with anti-lymphocyte antibody and complement caused a dose-dependent suppression of blastogenic response to purified protein derivatives (PPD). No effect, however, was noted on migration-inhibitory factor (MIF)-producing cells. In PWM-driven Ig synthesis, T lymphocytes lacking the anti-lymphocyte antibody-reactive T-cell subset enhanced PWM-driven Ig synthesis of autologous B lymphocytes. Con-A-induced suppressor function of lymphocytes was abolished by the treatment with anti-lymphocyte antibody and complement. The present study demonstrated that lymphocytes from normal individuals after treatment with anti-lymphocyte antibody and complement showed similar immunological reactivities with lymphocytes from active SLE, indicating that those anti-lymphocyte antibodies could play an important role in defective suppressor cell function.

Antibody-Dependent Cell Cytotoxicity↗

PubMed1994

The effects of thymopentin on the development of SLE-like syndrome in the MRL/lpr-lpr mouse.

Thymopentin (TP-5) is a synthetic pentapeptide that corresponds to the active 32-36 amino acid sequence of the thymic hormone thymopoietin, of which it retains all the immunomodulatory properties. In this study, we have evaluated the effects of long term prophylactic treatment with TP-5 on the clinical, immunological and histological parameters of the SLE-like syndrome that spontaneously occurs in MRL/lpr-lpr (MRL-lpr) mice. TP-5, administered (s.c.) to these mice at the doses of 1, 10 and 100 mg/kg, was given daily, five times a week, from the 9th to the 26th weeks of life. The prophylactic treatment with TP-5 prolonged in a clear dose-dependent fashion the lifespan of MRL-lpr mice as compared with PBS-treated control mice, and the effect reached statistical significance at the doses of 10 and 100 mg/kg. In parallel ex vivo studies, this clinical effect was associated with multiple profound modifications of the immune system including: (i) the reduction of the spontaneous and Con A-induced release of interleukin-4 (IL-4); (ii) the increased secretion of interferon-gamma (IFN-gamma) and IL-6 upon polyclonal mitogenic stimulation, and (iii) the amelioration of the defective Con A-induced lymphoproliferative response. In contrast, although the drug diminished the severity of proteinuria in MRL-lpr mice, it neither reduced histological signs of lupus nephritis nor diminished the serum titres of anti-native DNA and anti-histone autoantibodies. These results indicate that TP-5 displayed powerful immunodulatory activities in a well known model of human SLE.

Amino Acid Sequence↗

PubMed1988

HLA-A,B,C, and DR antigens, GLO I and Bf marker profiles in 75 Cape coloured patients with systemic lupus erythematosus (SLE).

HLA-A,B,C and DR antigens were tested in 75 Cape Coloured systemic lupus erythematosus (SLE) patients, and the GLO I and Bf markers in 51. The patients with HLA-DR2 had a relative risk significantly greater than one (p=0.0005). Twenty-two (29%) patients had only one detectable DR antigen. Of these, 11 (50%) were found to have DR2 only. The HLA-DR7 antigen was associated with severe disease (p less than 0.02). Bf and GLO I markers were not associated with SLE.

Complement Factor B↗

PubMed1992

Monoclonal large granular lymphocyte proliferation in SLE with HTLV-I seroreactivity.

A 60-year-old part Aboriginal woman was observed to develop severe neutropenia and a large granular lymphocyte (LGL) proliferation five years after the diagnosis of systemic lupus erythematosus (SLE). Monoclonality of the CD3+, CD4-, CD8+ LGL population was confirmed using the novel approach of X-linked restriction fragment length polymorphism (RFLP) analysis. Indeterminate HTLV-I serology was present. The patient responded to steroid therapy. LGL proliferation in the setting of SLE and the use of X-linked RFLP analysis to define LGL clonality have not previously been reported.

Antibodies, Monoclonal↗

PubMed1988

A new DNA immune adsorbent for hemoperfusion in SLE therapy: a clinical trial.

This investigation studied the preparation and clinical trial of DNA immunoadsorbent for hemoperfusion in systemic lupus erythematosus (SLE) therapy. DNA was complexed with blue tetrazolium (BT), then mixed with collodion, and finally adsorbed on macroporous spherical polymeric adsorbent. The percentage of DNA thus immobilized was 98-98.5%, and no release was detected during hemoperfusion. A patient with severe SLE was treated with the above adsorbent in hemoperfusion. The patient was in coma, with high anti-DNA antibody and abnormal immune complex levels, which fell sharply from 56.34% to 0.8% after 2.5 h of whole-blood hemo perfusion. There were no major clinical complications, and 2 weeks later, her proteinuria level became normal and immune complex levels were sustained. She was then discharged from the hospital and has been in good health for more than 1 year.

Adult↗

PubMed1983

Immunocompetent cells in labial salivary glands in secondary Sjögren's syndrome associated with SLE.

T and B lymphocyte (sub)populations were identified by monoclonal hybridoma antibodies (the avidin-biotin-peroxidase complex method), in the periductal lymphocyte-rich infiltrates in the labial salivary glands of 8 patients with secondary Sjögren's syndrome (2 degrees SS) associated with systemic lupus erythematosus (SLE). 59 +/- 7% and 17 +/- 3% of inflammatory round cells in situ were T3-positive and surface(SIg)- or cytoplasmic(CIg) immunoglobulin-positive, respectively. This suggests a local T lymphocyte dominance in salivary glands in 2 degrees SS associated with SLE. The local ratio of cells expressing T inducer/helper: T suppressor/cytotoxic phenotype was 3.5 +/- 0.8 (range 0.9-7.6) indicating large variations between individual patients. 46 +/- 9% of all inflammatory cells in situ were endogenous peroxidase-negative, Ia-positive cells, suggesting an active role for the locally accumulated T lymphocytes.

Adult↗

PubMed1997

Evaluating the neurocognitive complications of SLE. Lessons from HIV disease.

In this paper, we have attempted to define some of the theoretical, methodological, and practical issues involved in the use of NP testing to detect, classify, and monitor neurocognitive impairment secondary to systemic lupus erythematosus. We have drawn on experience with other clinical entities-primarily HIV disease-to inform this discussion. We have argued that for the purposes of studying NP-SLE, NP testing remains the gold standard and is also the most practicable approach in most settings, be they clinical or research. At the same time, the selection of NP tests must be carefully considered, particularly in a disease such as SLE in which the neurocognitive complications arise from several etiological mechanisms, affect people at various points in the course of disease, and in which the anatomic distribution of pathology in the brain varies from patient to patient. In this context, it is safest to select a test procedure that assesses all major areas of cognitive functioning with tests for which adequate demographically adjusted norms exist. In this way, a more reliable diagnosis of neurocognitive impairment, mild neurocognitive disorder, or dementia may be made. A reliable and valid neurocognitive diagnosis is the first step in monitoring patients clinically, in designing research aimed at neuropathogenesis, or in the design of treatment trials geared toward neuroprotection or neuroremediation.

Cognition Disorders↗

PubMed2003

CD137-mediated T cell co-stimulation terminates existing autoimmune disease in SLE-prone NZB/NZW F1 mice.

T cell receptor recognition of antigen and major histocompatibility complex (signal 1) and T cell co-stimulation (signal 2) are essential for full T cell activation, differentiation, and survival of naïve and activated T cells. The proto-typical T cell co-stimulatory receptor, CD28, is a constitutively expressed type I integral transmembrane protein and member of the Ig superfamily. Since its discovery, additional T cell co-stimulatory receptors have been identified, a number of which belong to the tumor necrosis factor receptor superfamily. Included within this group is CD137 (4-1BB), an activation-inducible, type I transmembrane protein. Co-stimulation of T cells through CD137 effectively up-regulates CD8 T cell activation and survival. Although CD4(+) T cells are efficiently activated through the T cell receptor and CD137 receptor, it provokes CD4(+) T cell anergy and blockade of T-dependent humoral immune responses. Therefore, we tested whether agonistic anti-CD137 monoclonal antibodies (mAbs) would be effective in blocking the induction or progression of B cell dependent autoimmune disease. Herein, we demonstrate the protective effect of agonistic anti-CD137 mAbs in blocking systemic lupus erythematosus (SLE) disease progression in NZB/W F1 mice. Protection from SLE following anti-CD137 mAb treatment is not confined to rescuing mice from disease progression; rather, it fully protects young mice from developing any symptoms of disease. We further found that treatment of proteinuric mice with anti-CD137 blocks ongoing anti-dsDNA autoantibody production.

Animals↗

PubMed1999

[A case of Chlamydia pneumonia and systemic lupus erythematosus (SLE) pleurisy].

A 40-year-old female was admitted with right chest pain. SLE was absent from her past history, although she complained of polyarthralgia in winter. Atypical pneumonia/pleuritis was suspected by chest X-ray film, showing a nodular shadow in the right lower field and moderate pleural effusion. Chlamydia pneumonia was diagnosed by elevated anti-C. psittsci antibody, while characteristics of pleural fluid revealed serositis accompanied by SLE because of the high titered anti-DNA antibody and the low titered complement. She was cured by clarithromycin and subsequent administration of prednisolone and cyclophosphamide.

Adult↗

PubMed2005

Proton magnetic resonance spectroscopy may predict future brain lesions in SLE patients: a functional multi-imaging approach and follow up.

OBJECTIVE: To determine whether single photon emission tomography (SPECT) and magnetic resonance spectroscopy (1H-MRS) can predict the appearance of new lesions in systemic lupus erythematosus (SLE), detectable by magnetic resonance imaging (MRI). METHODS: (99)Tc(m)-HMPAO-SPECT, brain MRI, and (1)H-MRS were done in eight women with SLE (mean age 31.8 years; disease duration 5.5 years). NAA/Cho, NAA/Cre, and Cho/Cre ratios were assessed in hypoperfused and normoperfused areas detected by SPECT that were normal on MRI examination. Reference values were obtained in 20 normal healthy controls. In five patients, MRI was repeated four to six years after the first evaluation. RESULTS: Mean NAA/Cho and Cho/Cre ratios in hypoperfused and normoperfused frontal areas were, respectively, lower and higher than control. There were no differences in NAA/Cre ratios. Mean Cho/Cre ratios were increased in hypoperfused v normoperfused brain areas (mean (SD): 1.43 (0.27) v 1.00 (0.07); p<0.023). NAA/Cre ratios were not altered (2.18 (0.30) v 1.99 (0.28); p = 0.381). Three of five patients who had a second MRI had new lesions in areas previously abnormal on MRS and SPECT but normal on first MRI. One patient with positive MRI, SPECT, and MRS showed an increase in the number of MRI lesions; one patient with negative MRI, SPECT, and MRS did not show any new lesions. CONCLUSIONS: Abnormalities reflecting altered perfusion or neuronal-chemical changes can be demonstrated by functional imaging techniques even in the absence of morphological lesions detectable by MRI. The abnormal areas identified by SPECT and MRS may predict future parenchymal damage.

Adolescent↗

PubMed1976

Avascular necrosis in SLE. An apparent predilection for young patients.

Recent reports of avascular necrosis (AN) in systemic lupus erythematosus (SLE) have suggested that its occurrence may be most frequent in young patients. In our population of 99 patients with SLE, 7 young patients have developed AN. Patterns of prednisone therapy had no apparent relationship to the development of AN. AN may become apparent in patients who have relatively inactive lupus, when increased physical activity precipitates articular collapse. A diagnosis of AN should be considered in young patients with localized joint pain.

Adolescent↗

PubMed1982

Prognostic value of anti-dsDNA in SLE.

In a prospective longitudinal study 130 patients with systemic lupus erythematosus (SLE) were studied at least monthly for a relationship between the anti-dsDNA levels and disease activity. We observed 13 patients who developed 15 periods of exacerbations of their disease. All 15 exacerbations were preceded by a continuous increase of the anti-dsDNA levels. In 13 of the 15 exacerbations studied the exacerbation was preceded by an increase of anti-dsDNA with a doubling time (T2) of less than 6 weeks; in 4 of the 5 other exacerbations the T2 was less than 10 weeks. Four other patients with an increase of the anti-dsDNA levels showed no exacerbation. In these 4 patients the T2 was larger than 10 weeks. The other 113 patients did not show an increase of anti-dsDNA over the 2 years of monitoring and showed no signs of serious disease activity (no major symptoms). These observations suggest that an SLE patient who is followed up frequently and who shows a continuous increase of anti-dsDNA witha T2 shorter than 10 weeks is bound to develop an exacerbation.

Antibodies, Antinuclear↗