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PubMed1992

Serological detection of disease activity in SLE.

Laboratory tests are commonly used to aid in monitoring disease activity in patients with systemic lupus erythematosus. Typically, tests for antinative DNA, complement, acute phase reactants, and sometimes circulating immune complexes are used for this purpose. More recently, tests for complement activation products and immunocyte activation have been suggested. We measured antinative DNA, C4, Westergren sedimentation rate, iC3b, Bb, and sIL-2R levels in a group of 100 patients with SLE evaluated clinically for activity by a modified version of the Systemic Lupus Activity Measure (SLAM); iC3b and Bb were studied in 71 of the patients and sIL-2R in 52. We found that sIL-2R and sedimentation rate correlated best with SLAM, anti-DNA was intermediate, and C4, iC3b, and Bb correlated the least. None of the tests predicted severity of disease, but sIL-2R was highest in patients with active renal disease.

Adolescent↗

PubMed1980

Colicin E1 plasmid as a probe for detection and study of anti-dna activity in SLE sera.

Tritiated colicin E1 plasmid DNA ([3H]DNA) was purified, characterized and developed as a test antigen for study of anti-DNA antibody activity in a modified Farr assay. The homogeneous molecular weight (4.2 X 10(6) daltons), physical state (intact covalently closed circles), and capacity for intrinsic radioactive labeling to a suitable specific activity were all important properties of the plasmid probe. In addition, the ability of the Farr assay to measure primary antigen/antibody interactions made quantitative determinations of anti-double-stranded DNA (dsDNA) antibody activity possible. Sonication of the plasmid resulted in definable fragments which were thermally denatured and used in the measurement of anti-single-stranded DNA (ssDNA) antibody activity. Results from studies in which unlabeled dsDNA, ssDNA, amd free 2'-deoxyribonucleotides were employed to inhibit binding of [3H]DNA by anti-DNA antibodies indicated the presence of 3 distinct anti-DNA specificities in SLE sera.

Antibodies, Antinuclear↗

PubMed1982

Enzyme-linked immunosorbent assay for antibodies to native DNA in sera of patients with SLE.

A micro-ELISA technique has been developed to measure antibodies to native DNA and used in SLE patients. The distribution of antibody to native DNA in the main immunoglobulin classes was studied, using anti-human globulin conjugates labelled with peroxidase. the antigen (double-stranded DNA from calf thymus) used in the assay was adsorbed to the surface of polystyrene plates treated with methylated bovine serum albumin. The standardization of the method was carried out by use of globulin calibration curves.

Adsorption↗

PubMed1983

Pharmacologic inhibition of experimentally induced SLE-like deposition of immunoglobulins in skin nuclei.

Binding of autologous immunoglobulins to epidermal nuclei can be induced in mice sensitized to ultraviolet-irradiated DNA following total body uv irradiation. The lesions, which resemble those observed in human systemic lupus erythematosus (SLE), are characterized histologically by the accumulation of polymorphonuclear (PMN) cells at different skin sites. In the present investigation this experimental model has been employed to study whether currently used anti-inflammatory (chloroquine, hydrocortisone, indomethacin) and polyvalent antiprotease (trasylol) drugs can either abolish or reduce the development of this murine pathology. The results of this study demonstrate that while trasylol, chloroquine, and indomethacin are able to inhibit, with variable effectiveness, the experimental skin lesions, hydrocortisone does not manifest any therapeutic activity.

Animals↗

PubMed1990

SLE and malaria: another look at an old idea.

An alternative view of the relationship between autoimmune disease and malaria is provided in the following article by Geoff Butcher and Ian Clark. Here they reassess the evidence that favours an earlier suggestion that where parasitic infections are common, autoimmune disease is rare. They suggest that malaria may exert a protective effect against the autoimmune nephritis in systemic lupus erythematosus (SLE).

Journal Article↗

PubMed1996

Human CD4-reactive antibodies from SLE patients induce reversible inhibition of polyclonal T lymphocyte proliferation.

We report on isolation of human polyclonal CD4-reactive antibodies of IgM and/or IgG isotypes from several SLE patients. These antibodies bound specifically to CD4-expressing cell lines and to rCD4 in ELISA and immunoblots. Saturation of CD4-binding sites occurred at antibody concentrations between 5 and 15 micrograms/ml. Anti-CD4 antibodies, in a dose-dependent manner, suppressed the proliferative responses of human peripheral blood mononuclear cells (PBMC) to superantigens (Staphylococcal enterotoxins A and B), anti-CD3 antibodies, and mitogens (PWM and Con A, but not PHA). They could also inhibit the proliferation of highly purified human T cells induced by immobilized anti-CD3 antibodies. To promote their effects on T cells, human anti-CD4 antibodies had to be present at lymphocyte cultures before or at the time of priming. There was no significant inhibition when antibodies were added more than 24 h following T cell activation. Substantial evidence that the immunosuppression induced by anti-CD4 antibodies was due to their direct effect on T cells was obtained. Down-regulatory effect of anti-CD4 antibodies could be significantly reversed by addition of exogenous IL-2 and by preincubation with soluble recombinant (r)CD4. Interestingly, at least one affinity-purified anti-CD4 antibody could costimulate the T cell proliferation induced by superantigens or anti-CD3 antibodies, especially when used at subsaturating concentrations (1-4 micrograms/ml) and when added subsequently to the initiation of cultures.

Autoantibodies↗

PubMed1988

Prognosis in SLE: comparison of Markov model to life table analysis.

A Markov model of prognosis was evaluated by comparing the duration of disease activity states and life expectancy with Kaplan-Meier survival curves for 98 patients with systemic lupus erythematosus with 1080 patient-years of observation. A four state (remission, active, flare and death) homogeneous Markov chain was constructed to determine the transition probabilities between disease states, the probability of disease states over the subsequent 25 years, time in each disease state, and life expectancy. Approximately 85% of the clinical course of patients was in the active disease state; no patient made a transition directly between remission and flare; virtually all deaths occurred from the flare disease state. The proportion of the patient population in each disease state over time provided a convenient graphic summary of the natural history of SLE that supplemented the Kaplan-Meier survival curves. A Markov model analysis yields a clinically useful description of outcome for multistate diseases that supplements survival curves.

Actuarial Analysis↗

PubMed2004

The immune response to cell death in SLE.

Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterized by the production of antinuclear antibodies (ANA). These antibodies target a wide variety of antigens whose presence in an immunologically active form may result from cell death processes that cause their translocation and release from cells. As indicated by in vivo model systems, the release of DNA from cells may not be a simple consequence of cell death but rather may require the intervention of other cell types including macrophages. Thus, in mice, administration of either apoptotic or necrotic cells produces a blood DNA response, whereas mice lacking macrophages fail to show blood DNA under the same conditions. Furthermore, the circulating DNA arising from apoptotic and necrotic cells displays a similar pattern with respect to size distribution, with both showing DNA laddering, a pattern indicating enzymatic cleavage. Since circulating DNA in the form of immune complexes can play a role in lupus pathogenesis, these findings suggest that the generation and clearance of dead cells are important events that may underlie autoimmunity in this disease and may be targeted for therapy.

Animals↗

PubMedDate not supplied

Mice with a regenerative wound healing capacity and an SLE autoimmune phenotype contain elevated numbers of circulating and marrow-derived macrophage progenitor cells.

Mice from the MRL strain are prone to develop systemic lupus erythematosus (SLE) and have demonstrated accelerated wound healing and scarless tissue regeneration; however, many of the mechanisms involved in these clinically relevant pathologies are unclear. Prior studies have described macrophage accumulation and functional defects in mice prone to lupus. Monocyte-macrophages have also been shown to have a high degree of plasticity. To determine whether there might be innate differences in the hematopoietic systems of MRL mice, we evaluated hematopoietic progenitor cell content in a variety of tissues and the proliferative responses of derived marrow and thioglycolate (TG)-elicited peritoneal macrophages. Our experiments reveal that MRL mice have significantly lower numbers of circulating blood leukocytes and platelets. Even more strikingly, we found that MRL blood and marrow contain an unusually robust number of unique and assayable macrophage colony-stimulating factor responsive cells which have the characteristics of macrophage colony-forming cell precursors. In culture, in contrast to cells derived from control C57BL/6 mice, this cell type and thioglycolate-elicited peritoneal macrophages from MRL mice can be extensively expanded with just macrophage colony-stimulating factor to acquire an in situ "f-mac-like" (see Y. Zhao, D. Glesne and E. Huberman, A human peripheral blood monocyte-derived subset acts as pluripotent stem cells. Proc. Natl. Acad. Sci. U.S.A. 100, (2003) 2426-2431.) morphology when plated on plastic surfaces. Our results suggest that these increased numbers of macrophage progenitor cells and their potential differentiation plasticity may play a functional role in the onset of systemic lupus erythematosus and may also contribute to the accelerated and scarless tissue regenerative repair response observed in MRL mice.

Animals↗

PubMed2005

Comparison between sample disruption methods and solid-liquid extraction (SLE) to extract phenolic compounds from Ficus carica leaves.

Sea sand disruption method (SSDM) and matrix solid phase disruption (MSPD) were compared to solid-liquid extraction (SLE) for extraction of phenolic compounds from the Ficus carica leaves. Statistical treatment, ANOVA-single factor, was used to compare the extraction yields obtained by these methods, and for the majority of the extracted compounds, significantly higher yields were obtained by the solid disruption methods. Both solid disruption methods are faster and ecologically friendly, but the sea sand method was more reproducible (RSD < 5% for most compounds), and was also the least expensive method. Recoveries above 85% were obtained for chlorogenic acid, rutin, and psoralen using the sea sand extraction method.

Chemical Fractionation↗

PubMed2006

Treatment with rituximab affects both the cellular and the humoral arm of the immune system in patients with SLE.

Herein we investigated how rituximab-induced B cell depletion affected leukocyte subpopulations and antibody titers in SLE patients. We focused our analysis on time points related to absence and return of B cells after depletion. A correlation was found between the baseline frequency and time to repopulation; the fewer B cells initially, the longer to their return. While the few B cells remaining after treatment were of memory, double-negative (IgD-CD27-), and CD5+ phenotype, the returning B cells were mainly naïve, indicating de novo production of B cells. Serum levels of IgG and antibodies against Ro52, Ro60, La44, measles and tetanus remained unchanged, while decreases in IgM, IgE, anti-dsDNA and anti-C1q antibodies were observed. Additionally, a significant increase in activated CD4+ and CD8+ T cells, as well as CD25bright FOXP3+ regulatory T cells was observed. In conclusion, both the humoral and the cellular immune systems were affected by treatment with rituximab.

Antibodies, Monoclonal↗

PubMed2005

SLE: translating lessons from model systems to human disease.

Systemic lupus erythematosus (SLE, lupus) results from immune-mediated damage to multiple organs. Its pathogenesis should be viewed as a series of steps, beginning with impaired immune regulation that permits self-reactive T-B-cell activation, which results in the production of autoantibodies. Activated T and B cells then infiltrate tissues, which along with autoantibody and immune complex deposition, triggering local events that ultimately cause organ damage. Although improved understanding of early autoimmune events might open up avenues for disease prevention, future investigations must focus on the mechanisms of end-organ damage in model systems and how to translate this knowledge into human disease. Understanding the mechanisms of each pathogenetic step would provide a rational basis for the development of disease stage-specific diagnostic markers and treatments.

Animals↗

PubMed2000

Effect of systemic lupus erythematosus (SLE) treatment drugs on GI-101A breast tumor cell growth.

The effect of systemic lupus erythematosus (SLE) treatment drugs on PKC (protein kinase C) activity and cell growth was studied using GI-101A breast tumor cells. Both hydroxychloroquine (HCQ) and prednisone treatments significantly increased the PKC activity in GI-101A cells after 60 min. Treatment of cells with a combination of HCQ/prednisone also produced the highest increase in PKC activity following 60 min incubation. When the GI-101A cells were treated with the same drugs, HCQ (10 ng/ml) prednisone (10 ng/ml) and HCQ/prednisone combination (10 ng/ml of each), for 72 hr the total PKC activity in the cells was significantly elevated and consequently the GI-101A cell growth was stimulated. As a result of drug induced cell growth stimulation the total number of cells in the treatment groups increased significantly compared to the non-treated controls. Interestingly HCQ and prednisone treatment induced cell growths were completely blocked by PKC specific inhibitor chelerythrine (50 microM). Our results suggest that HCQ and prednisone treatment can induce GI-101A cell growth via activating PKC.

Breast Neoplasms↗

PubMed1982

Diet-induced systemic lupus erythematosus (SLE) in primates.

Ten adult, female cynomolgus macaques were randomly assigned to two equal groups: (1) semipurified diet (SPD); and (2) SPD with 45% ground alfalfa seed (AS). Both groups were studied at monthly intervals after 5 mo on their respective diets. Control animals had a mean hematocrit (Hct) of 43 +/- 2%, negative antiglobulin (AG), antinuclear antibody (ANA) and LE cell tests. Mean values for C3 and C4 were 309 +/- 47 mg/dl and 35 +/- 7 mg/dl, respectively. Mean serum binding to radiolabeled double stranded deoxyribonucleic acid (dsDNA) was 1.9 +/- 0.2%. Three of five animals fed AS developed signs of an SLE-like illness characterized by AG-positive anemia (lowest Hct 30%), positive ANA (highest titer greater than 1:15, 360; rim pattern) and elevated anti-dsDNA binding (highest 96%) with variable degrees of hypocomplementemia. One animal had granular deposition of immunoglobulin and complement at the dermal-epidermal junction of clinically normal skin the presence of immune complex-induced glomerulonephritis.

Animals↗

PubMed2000

Acute cerebellar ataxia of a patient with SLE.

We described a 28-year-old woman with systemic lupus erythematosus (SLE) presented with digestive tract, skin and renal symptoms and afterwards developed acute cerebellar ataxia, a paresis of the right inferior rectus muscle, left abducens paralysis and left facial palsy which seemed to be consistent with a brainstem lesion visible on magnetic resonance imaging (MRI). This lesion disappeared within 9 days of corticosteroid treatment. It is suggested that this lesion is focal edema induced by acute changes in the blood brain barrier secondary to a vasculopathy. Other causes, including local infarction, are unlikely.

Acute Disease↗

PubMed1998

Infections in nonleukopenic compromised hosts (diabetes mellitus, SLE, steroids, and asplenia) in critical care.

Acutely ill patients who are immunocompromised but not neutropenic most commonly are: (1) diabetic; (2) on chronic high-dose steroid therapy; (3) have lupus; or (4) have impaired or absent splenic function. These patients often present in the CCU because of the severity of their infection. Differential diagnosis may be approached by first considering the patient's underlying disease, i.e., SLE. The next step in the diagnostic process is to appreciate the immune defect associated with these disorders. The nature of the immune defect determines which clinical pathogens are related to the immune defect. Pathogens are associated with a sterotyped pattern of organ involvement. The object of the diagnostic analysis is to determine the most likely organism affecting a particular organ system, given the defect in host defenses associated with the patient's underlying illness. In this way, a useful clinical diagnosis can be made rapidly, and appropriate clinical specimens obtained for diagnostic testing. Often empiric therapy must be started pending the results of diagnostic testing. In such situations, empiric therapy ordinarily is directed against the bacterial pathogens most likely to cause disease relevant to the patient's impaired defenses. Specific therapy for unusual or exotic pathogens should not be empiric and should be based on demonstration of a pathogenic role by the microorganism. In the case of miliary tuberculosis or invasive fungal disease, a case may be made for early empiric therapy to cover these organisms if there is sufficient clinical suspicion based on the presenting signs and symptoms as well as the pattern of organ involvement. As with all infections, but particularly in immunocompromised patients, the early initiation of appropriate antimicrobial therapy is essential and often life-saving.

Adrenal Cortex Hormones↗

PubMedDate not supplied

Partial deficiency of the fourth component of human complement (C4) and autoantibody directed against C4 in a patient with SLE.

The finding of dramatically depressed levels of C4 in a 17-year old patient with severe systemic lupus erythematosus (SLE) prompted a genetic study of her family. This study revealed the existence of a partial C4 deficiency; we found the presence of a C4A3,C4BQo haplotype which was transmitted by the mother to each of her children. This patient possessed, in her serum, an autoantibody with anti-C4 specificity. The immunochemical characterization of this autoantibody revealed that it was IgM and belonged to the immunoconglutinin family. We have studied the effects of this autoantibody on the formation and dissociation kinetics of classical C3-convertase.

Adolescent↗

PubMed2003

Finding genes for SLE: complex interactions and complex populations.

Many years of work, multiplex family collection and endless genotyping finally give fruit. The original aim cannot be lost. The aim is not only to identify mutations involved in susceptibility for systemic lupus erythematosus (SLE) but to elucidate the disease pathogenesis as well. After genetics comes the biology. We review our recent findings on the genetics of lupus, provide possible mechanisms for disease susceptibility and present some facts on the problematic of identifying susceptibility mutations for complex diseases in complex human populations.

Antigens, CD↗