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PubMedDate not supplied

Kinetic analysis of immune complex solubilization: complement function in relation to disease activity in SLE.

Solubilization of preformed bovine serum albumin (BSA) rabbit anti-BSA complexes in serum with kinetic analysis, haemolytic complement function, complement proteins C1q, C4, C3 and complexes containing C1 inhibitor (C1 INH-C1r-C1s-C1 INH) were serially investigated in relation to disease activity in 25 patients with systemic lupus erythematosus (SLE). Clinical assessment of disease activity was expressed using a validated global index (SLEDAI). Markedly decreased capacity to solubilize immune complexes in serum was mainly found in sever disease. By serial analysis, evidence of fairly persistently impaired classical pathway function was found in most of the patients. In partial contrast, impaired alternative pathway function was more clearly associated with active severe disease. Immune complex solubilization during short incubation (5-10 minutes) correlated with classical and alternative pathway-mediated haemolysis. Solubilization during long incubation (40 minutes) was correlated with haemolytic alternative pathway function. In some patients gradual impairment of solubilization during short incubation, and reduced classical pathway haemolytic activity were detectable 2-4 months before clinical manifestations prompted therapeutical intervention. SLEDAI was negatively correlated with solubilization during prolonged incubation (40 minutes) and with haemolytic alternative pathway function, further emphasizing involvement of the alternative pathway in severe disease. The findings emphasize the importance of impaired complement function due to complement activation in SLE. Assays for immune complex solubilization or other complement functions appear to be useful for monitoring disease activity in SLE.

Antigen-Antibody Complex↗

PubMed1992

[A case of systemic lupus erythematosus (SLE) developing pan-dysautonomia].

A 43-year-old woman who had been diagnosed as primary Sjögren's syndrome since 1986 developed severe constipation, urinary retention, dizziness at standing and polyarthralgia in February, 1990. Laboratory tests revealed proteinuria, hypocomplementemia and high titer of anti-DNA antibody. Diagnosis of SLE was made and she was admitted to our hospital on April 2, 1990. Physical examination on admission showed that she also had asymmetric pupils, impairment of sweating, orthostatic hypotension, neurogenic bladder, gastro-intestinal dysmotility and the diminution of R-R interval variability during deep breathing on the electrocardiogram. These findings suggested that she had pan-dysautonomia but there were no signs of motor and sensory disturbance. Because other diseases such as diabetes mellitus and amyloidosis which induced dysautonomia could be ruled out, her pan-dysautonomia seemed to be due to SLE. After the treatment with steroid pulse therapy, most of her dysautonomia improved rapidly. However, some of the disturbance had persisted for a long time. Pan-dysautonomia has been rarely reported as a complication of SLE, and high dose of steroid therapy at the early stage should be considered.

Adult↗

PubMed2006

[Neurological or psychiatric symptoms in patients with systemic lupus erythematosus (SLE): terminological problems, pathogenesis, diagnosis and therapy].

The nomenclature of the American College of Rheumatology leads to misunderstandings in multidisciplinary discussions on patients with systemic lupus erythematosus (SLE) who also have neurological or psychiatric symptoms. These proposed neuropsychiatric syndromes are rarely syndromes and the symptoms are rarely neuropsychiatric. It is better first of all to determine whether the SLE patients have neurological or psychiatric symptoms, and if these symptoms are present, the first question is what is the cause. Vasculitis of the cerebral blood vessels should be considered as a possible explanation only if ischaemic lesions in the brain have been demonstrated, other causes of cerebral ischaemia in SLE are unlikely, and the clinical signs are consistent with cerebral vasculitis. These other causes of cerebral ischaemia include: antiphospholipid antibodies, atherosclerosis, heart valve disorders and thrombotic thrombocytopenic purpura.

Brain↗

PubMed2006

Th1/Th2 balance of SLE patients with lupus nephritis.

Systemic lupus erythematosus (SLE) is a prototypic systemic autoimmune disease that is characterized by the production of multiple autoantibodies and immune complex formation. Lupus nephritis, which has various histological patterns and variable clinical outcomes, is one of the most important complications of SLE. Although this pathogenetic mechanism in each histologically different type of nephritis remains unclear, recent findings in murine lupus elucidate an essential role for the Th1 cytokine in the development of diffuse lupus nephritis (DLN), and Th2 cytokine in that of membranous lupus nephritis (MLN). These data support the hypothesis that individual Th1/Th2 balance is one of the critical determinants for histopathology of lupus nephritis. Therefore the value of Th1/Th2 ratio of the peripheral CD4+ T cells in SLE patients could be a useful index to predict histopathology of lupus nephritis.

Animals↗

PubMed1991

Immunoglobulin allotypes in systemic lupus erythematosus--results of a central European multicenter study. SLE Study Group.

Immunoglobulin heavy chains (G1m, G2m, G3m, A2m) and kappa light chain (Km) allotype and phenotype frequencies were examined in 323 central European Caucasian patients with systemic lupus erythematosus (SLE). No significant differences were found between the different allotype or phenotype frequencies of the SLE patients and a control group of healthy individuals. Our results indicate that Gm, A2m and Km allotypes do not represent susceptibility factors for SLE in Caucasians.

Gene Frequency↗

PubMed1991

[Serum level of beta-glucuronidase as potential indicator of disease activity in rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE)].

The lysosomal enzyme beta-glucuronidase is involved in the degradation of glycosaminoglycans to monosaccharides. beta-glucuronidase-activity has been found to correlate well with histomorphological changes in active arthritis. By use of a new--enzyme kinetic--assay serum activity of beta-glucuronidase was measured in 32 patients with rheumatoid arthritis (RA) and 23 patients with systemic lupus erythematodes (sLE) and compared to 120 healthy volunteers. In 72% of the patients with RA and 65% of the patients with sLE increased beta-glucuronidase-activity was found (greater than 97.5. percentile of healthy volunteers). There was no correlation with an estimated score of disease activity, duration of morning stiffness, or blood sedimentation rate. The determination of beta-glucuronidase revealed increased serum levels in most of the patients with RA and sLE. The role of beta-glucuronidase as a predictor of joint destruction remains to be evaluated in a prospective study. For this evaluation the use of the enzyme-kinetic method described here is recommendable.

Adult↗

PubMed1987

Erythrocyte complement receptor type 1 (CR1) expression and circulating immune complex (CIC) levels in hydralazine-induced SLE.

Family studies were carried out to look at CR1 expression in 24 hydralazine-induced SLE patients (Hz Reactors), who had been off the drug for at least 1 year and were clinically well at the time of the study. Mean expression of CR1 was reduced by 27% in the group of hypertensives who had developed Hz-induced SLE compared with a group of 35 normal individuals. CR1 expression was also slightly reduced in the relatives of the Hz Reactors compared to the normal group. Using a solid-phase Clq binding assay, CIC levels were found to be elevated in the plasma of the Hz reactors and an inverse relationship was found between CR1 levels and CIC levels in this patient group. Both CR1 levels and CIC levels in Hz Reactors and normal individuals were constant over the 36 weeks studied. This study suggests that there is an association between an inability to deal efficiently with CIC and susceptibility to developing Hz-induced SLE.

Antigen-Antibody Complex↗

PubMed1987

Erythrocytes transfused into patients with SLE and haemolytic anaemia lose complement receptor type 1 from their cell surface.

Erythrocyte complement receptor type 1 (CR1) shows a numerical deficiency in patients with SLE and with haemolytic anaemias. This receptor is a cofactor for the enzymatic degradation of C3b and is believed to play a role in the transport of immune complexes from the circulation to the reticulo-endothelial system. Erythrocyte CR1 was enumerated on cells which had been transfused into patients with SLE and haemolytic anaemias. In three patients with active disease up to 60% of CR1 was lost from erythrocytes during 5 days after blood transfusion and up to 410 molecules of C3 were deposited on these cells. These are the first in vivo data showing that CR1 may be lost from circulating erythrocytes. This acquired deficiency of CR1 on erythrocytes may have pathological consequences in patients with SLE.

Anemia, Hemolytic, Autoimmune↗

PubMed1988

C3b receptor (CR1) on phagocytic cells from SLE patients: analysis of the defect and familial study.

In vitro CR1-dependent phagocytosis of C3b-coated erythrocytes, by monocytes and PMN, was found to be significantly decreased in SLE patients. This was in many cases related to a specific defect of CR1 receptors, since the FcR-ingestion of EIgG was normal. On the other hand, CR1 levels of PMN stimulated by FMLP were also found to be decreased in SLE patients, while both the expression of circulating PMN (cells isolated at 4 degrees C) and the total cellular CR1 content were normal. On the basis of the available data, we propose that the impaired phagocytosis is due to a functional defect of CR1 or a defective anchorage of the receptor to the plasma membrane, possibly related to the decreased capacity of CR1 to be up-regulated by FMLP. To study the importance of the genetic background in the CR1 abnormalities, the families of 22 young SLE patients, in which the onset of the disease had occurred before the age of 15, were studied. The expression of CR1 on erythrocytes, and the total CR1 content of PMN, in parents and siblings of these patients did not differ significantly from normal controls. By contrast, the ingestion of EIgGC3b by PMN from healthy relatives of these patients was decreased (65% of the normal mean of PI), while EIgG phagocytosis was normal. A relation between this CR1 functional defect and the familial occurrence of autoimmune disorders is therefore possible.

Erythrocytes↗

PubMed1986

Mononuclear phagocyte function in SLE. I. Bipartite Fc- and complement-dependent dysfunction.

To determine the relative contributions of Fc- and complement-mediated immune clearance to the overall mononuclear phagocyte system (MPS) dysfunction in SLE, we performed a kinetic analysis of clearance rate data from 32 patients and 49 normal controls. Three rate constants regulating complement-mediated MPS clearance and one rate constant regulating Fc-mediated MPS clearance were evaluated. Mean values for rate constants regulating complement-mediated phagocytosis (k4) and Fc-mediated clearance (k3) were significantly lower for the patient population as a whole when compared with normal controls (p less than 0.01 and p less than 0.001, respectively). Further analysis by clinical subgroups revealed that mean k3 values were significantly low for all but the inactive nonrenal subset of patients, whereas mean k4 values were significantly low for both the active and inactive renal patients but not for nonrenal patients. Rate constant values for Fc-mediated clearance correlated significantly with disease activity scores for the entire SLE group (p less than 0.001) as well as for the subset of patients with active and inactive renal disease (p less than 0.001). Neither k3 nor k4 correlated significantly with anti-DNA antibody, titers, total hemolytic complement levels, or circulating immune complexes. These data indicate that both Fc- and complement-mediated clearance defects occur in SLE. Nonrenal patients have at least one clearance mechanism intact, whereas immune complex glomerulonephritis is associated with dysfunctions in both of these clearance mechanisms.

Adult↗

PubMed1986

The role of nonactivated and interferon-gamma activated monocytes in regulating normal and SLE patient B cell responses to TNP-Brucella abortus.

We have previously characterized the human B cell response to trinitrophenol (TNP)-Brucella abortus (Ba) response as being T cell independent. In this report we examine the role of monocytes in the TNP-Ba antibody response of human peripheral blood mononuclear cells (PBMC). Depletion of monocytes by sequential adherence to plastic and Sephadex G-10 passage did not result in decreased plaque-forming cell responses to TNP-Ba, suggesting that monocytes were not required. On the contrary monocytes were probably inhibitory because their removal resulted in enhanced responses. This was confirmed by showing that adding monocytes back reconstituted the inhibition. When interferon-gamma (IFN-gamma), a potent activator of monocytes, was added to TNP-Ba-driven PBMC cultures, marked inhibition (greater than 90%) of the responses ensued. This IFN-gamma-mediated suppression was monocyte dependent because it was completely abrogated by monocyte, but not T cell depletion. Previously, we described a concanavalin A (Con A), T cell inhibition pathway of the TNP-Ba response. Both the Con A and IFN-gamma pathways were tested for their ability to inhibit systemic lupus erythematosus (SLE) patient responses to TNP-Ba. The B cell response of SLE patients was inhibitable by both pathways. In all of the patients, the inhibition was complete (greater than 95%) when IFN-gamma was added to the cultures. In the presence of Con A, greater than 95% inhibition was observed in six of 10 patients, the remainder being inhibited to a lesser extent. Thus the hyperactive B cells from SLE patients can be down-regulated, particularly in the presence of IFN-gamma.

B-Lymphocytes↗

PubMed1986

Evaluation of the cross-reaction between anti-DNA and anti-cardiolipin antibodies in SLE and experimental animals.

The cross-reaction between anti-DNA and anti-cardiolipin IgG antibodies and its relation to the standard test for syphilis was studied with sera and monoclonal antibodies derived from human patients and mice with systemic lupus erythematosus (SLE). Syphilitic sera of humans and rabbits infected with the spirochete Treponema pallidum were also tested in this study. In addition, rabbits were immunized with ssDNA and cardiolipin and the cross-reactions of the induced antibodies were studied in two different assay systems. The results of these experiments suggest: that the anti-DNA and anti-cardiolipin IgG autoantibodies in SLE sera constitute separate antibody populations and, therefore, cardiolipin cannot play a role in the induction of immune response to DNA in SLE; that in immunized experimental animals there is a significant level of cross-reaction between anti-DNA and anti-cardiolipin-the detection of this cross-reaction depends on highly amplified solid phase assay systems which measure low affinity antibodies and that there is no correlation between the activity of syphilitic sera in the serologic test for syphilis and their binding to pure cardiolipin-this implies that cardiolipin may not be the dominant ingredient in this test as previously proposed.

Animals↗

PubMed1987

[A possible role of T cell subsets causing anemia in systemic lupus erythematosus (SLE)].

The influences of T cell subsets on erythropoiesis were studied in ten SLE patients with anemia of unknown etiology. In these SLE patients CFU-E growth from bone marrow mononuclear cells was significantly decreased compared with normal controls. However, an increase in CFU-E growth was resulted by the depletion of T cells or cytotoxic/suppressor T cells from bone marrow mononuclear cells with treatment of OKT3 or OKT8 monoclonal antibody in three out of the ten patients. Autologous peripheral blood mononuclear cells inhibited CFU-E growth by co-culture methods in three out of the ten patients. The inhibition of CFU-E growth was diminished by the depletion of OKT8+ T cells from peripheral blood mononuclear cells in one out of the three patients. After the corticosteroid therapy, in two patients, the suppression of CFU-E growth by peripheral blood mononuclear cells was significantly reduced in accord with recovery of anemia. It is assumed that T cells with inhibitory action to CFU-E growth belonging to OKT8+ subsets are present in some SLE patients with anemia and may play a pathogenetic role in the development of anemia.

Adult↗

PubMed1987

Autoantibodies to purified nuclear proteins related to DNA metabolism during ageing and in SLE patients.

In this study the specificity of circulating autoantibodies in ANA+ aged donors, ANA- donors and SLE patients was investigated by immunoblotting on total nuclear proteins and by ELISA on purified nuclear proteins, possibly related to DNA metabolism, such as DNA polymerase alpha, DNA-dependent ATPase, DNA Topoisomerase I, ssDBP, hnRNP, HMG and histones. Immunoblotting showed that sera from ANA+ aged donors present fewer antibodies to nuclear proteins, especially to those between 21,000 and 45,000, molecular weight (MW), than sera from SLE patients. When the specificity of antisera was further studied on purified nuclear proteins, it was found that the majority of sera from SLE patients react with most of the proteins tested, whereas sera from ANA+ aged donors mainly react with DNA polymerase alpha, DNA-dependent ATPase, DNA Topoisomerase I and histones. In addition, sera from a few ANA- donors also reacted with certain purified nuclear proteins in a statistically significant age-related manner.

Adolescent↗

PubMed1986

A comparison of three anti-double stranded DNA antibody assays on sera from SLE and other diseases.

Systemic lupus erythematosus (SLE) is a multisystem disorder accompanied by a diverse spectrum of serum autoantibodies. Antibodies to double stranded DNA (dsDNA) are considered to be the most specific marker for this disease. In this study the results obtained from three different assays for dsDNA are compared: an indirect fluorescence antibody assay (IFA), a radioimmunoassay (RIA) and, an enzyme-linked immunosorbent assay (ELISA), on 57 SLE sera and 28 Sera from other disorders. Correlation of these anti-DNA results are made with C3, C4, and antinuclear antibody (ANA) titers. Our results show the IFA assay is the most sensitive and the least specific of the three tests. The RIA was found to be the most specific and was approximately as sensitive as the ELISA. We also found significant inverse correlations between anti-dsDNA levels and circulating complement levels among SLE sera for all three assays. ANA titers were significantly correlated with all anti-dsDNA assays as well. However, these anti-dsDNA assays show only modest differences explainable by numerous mechanisms. Hence, a clearly superior anti-dsDNA method does not emerge from our study.

Antibodies, Antinuclear↗

PubMed1979

Complement-fixing anti--double-stranded DNA with the Crithidia method: a better indicator of active SLE than anti-DNA with the Farr method.

Twenty-seven patients with SLE of juvenile onset were studies for 2 years. Episodes of active disease and quiescence were defined and were related to levels of anti-dsDNA and C3. Two methods for the detection of anti-dsDNA--the Farr assay and Cr immunofluorescence--were compared. The latter method was also used to differentiate anti-dsDNA according to its Ig class and its CF property. Positive tests for anti-dsDNA and low C3 levels were correlated with activity of the disease. Results with the Farr assay and Cr Ig test were comparable, but both low C3 and Cr CF anti-dsDNA showed a significantly stronger association (p less than 0.001) with active SLE than did DNA binding by the Farr method or Cr Ig anti-dsDNA. Furthermore, in six patients followed during active disease and remission, a negative Cr CF test was the earliest sign of ensuing clinical remission; DNA binding and C3 levels took weeks to months longer to normalize. This predictive value of CF anti-dsDNA may be useful in monitoring therapy for SLE, especially if symptoms due to prior renal damage may be confused with active disease as in lupus nephritis.

Adolescent↗

PubMed1986

Renal biopsy in SLE irrespective of clinical findings: long-term follow-up.

We analyzed data from 56 patients with Systemic Lupus Erythematosus (SLE) in whom renal biopsies were done systematically. The data taken into account for the study were: the histologic glomerular lesions at diagnosis, serum creatinine value, degree of proteinuria and qualitative urine sediment analysis at the time of biopsy, patient age at diagnosis and the evolution of renal function until the time the study was made. Therapy was prescribed according to the glomerular histologic lesion. The mean follow-up period from the time of the first biopsy was 8.2 years. At the time of the study, only 3 patients (5.3%) were on dialysis, while the rest of the patients (94.7%) had a satisfactory renal function. Our results indicate that systematic renal biopsy in SLE patients can furnish valuable data concerning the renal status whether there are clinical signs of renal involvement or not. Treatment based on the histologic images alone may considerably improve renal survival in SLE.

Adolescent↗

PubMed1985

Antibodies to vimentin intermediate filaments in sera from patients with SLE and RA: quantitation by solid phase radioimmunoassay.

A solid phase radioimmunoassay was used to quantify levels of antibodies to vimentin intermediate filaments (VIF) of the cytoskeleton in sera from patients with systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). Significantly higher levels of these antibodies were found in 52% of the SLE sera studied, compared to 6% in RA sera and 10% of sera from healthy controls. These antibodies include IgG and IgM classes of immunoglobulins. Our results show that high levels of anti-VIF antibodies are more prevalent in SLE sera, whereas no significant differences are found between sera from patients with RA and healthy controls.

Adult↗