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PubMed1993

Epitope mapping of histone 5 (H5) with systemic lupus erythematosus, procainamide-induced lupus and hydralazine-induced lupus sera.

To define the linear epitopes on H5 that react with systemic lupus erythematosus (SLE) and drug-induced lupus (DIL) sera, concurrent overlapping hexameric peptides corresponding to the sequence of H5 were synthesized by stepwise elongation of the polypeptide chains on polyethylene supports. The hexapeptides were tested for reactivity with 8 SLE and 8 DIL sera using an enzyme linked immunosorbent assay (ELISA). SLE and hydralazine-induced lupus (HIL) antibodies were most reactive with peptide 45 (SSRQSI) and patients with procainamide-induced lupus (PIL) were most reactive with peptide 24 (SHPTYS). The epitopes of highest reactivity were in the globular domain of H5. Low reactivity was observed with carboxyl terminal peptides. These findings differ from immunoblotting studies of protease cleaved peptides which have previously shown that the H5 determinants are in the carboxyl terminus.

Amino Acid Sequence↗
PubMed1986

Impaired T-cell-independent B-cell maturation in systemic lupus erythematosus: coculture experiments in monozygotic twins concordant for Klinefelter's syndrome but discordant for systemic lupus erythematosus.

In a case of monozygotic twins discordant for systemic lupus erythematosus (SLE), coculture experiments with isologous (i.e., genetically identical) lymphocytes were performed. Adequate T-helper-cell function in the SLE twin was demonstrated. Lack of B-cell responsiveness to T-cell-dependent and T-cell-independent polyclonal activators points to a T-cell-independent B-cell maturation defect in the SLE twin.

Adolescent↗
PubMed2004

The potential pathogenetic link between peripheral immune activation and the central innate immune response in neuropsychiatric systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is an autoimmune disease of unknown etiology. Neuropsychiatric disturbances unexplained by drugs or by other untoward manifestations of disease are present in up to one-half of SLE patients and have profound economic and social impact. In patients with neuropsychiatric SLE, structural lesions have been identified in the hippocampus and proinflammatory cytokines have been detected in the cerebrospinal fluid. Similarly, murine models of lupus, such as MRL-lpr/lpr mice display behavioral disturbances which map to the hippocampus and exhibit overexpression of proinflammatory cytokine genes in hippocampal homogenates. Neuropsychiatric SLE typically occurs in the presence of serologically and clinically active lupus. In animal models of SLE, such as MRL-lpr/lpr, NZB, BXSB, and [NZB x NZW]F(1), uncontrolled autoreactivity in the periphery is accompanied by behavioral disturbances that are chronic and progressive. These observations suggest the hypothesis that central nervous system disease in SLE is driven by cross-talk between the peripheral immune system and the brain's innate immune system, which results in the inexorable activation of astrocytes, microglia, and/or neurons within the hippocampus. This leads to overproduction of brain cytokines, which induce the synthesis of pro-oxidant molecules, such as eicosanoids and reactive oxygen species, with resultant tissue injury. The cascade becomes self-perpetuating and eventuates in neuronal death, which is followed by impaired cognition. A better understanding of the molecular events that operate in the pathogenesis of neuropsychiatric SLE may provide the basis for a more rational therapeutic approach to this incompletely understood disease.

Animals↗
PubMed2003

Silent nephritis in systemic lupus erythematosus.

Silent lupus nephritis (SLN) was investigated in 42 renal asymptomatic patients and compared with 49 untreated patients with overt lupus nephropathy (OLN). Urinary sediment, quantitative proteinuria, creatinine clearance, antinuclear antibodies (ANA), complement, circulating immune complexes (CIC) and renal biopsies were evaluated in all of the patients. Forty-one out of the 42 (97.6%) patients had SLN according to histopathological findings. Results showed that the mean age, female/male ratio and the clinical activity index (SLEDAI) were similar in both groups (P > 0.05). The prevalence of ANA, anti-ds DNA, anti-ENA autoantibodies and C4 serum levels showed no statistical differences between the two groups (P > 0.05). Conversely, in the OLN group, elevated CIC and diminished CH50 and C3 serum levels were significantly different (P < 0.01). WHO class II was the predominant renal lesion in the group with SLN (P < 0.0001), whereas class IV was in the OLN patients (P < 0.0001). We conclude that, in our series, SLN was highly prevalent in renal asymptomatic patients with otherwise systemic lupus erythematosus. Furthermore, abnormal levels of CIC, CH50 and C3 associated with WHO class II suggest a moderate but ongoing activation of immune-mediated renal injury mechanisms.

Adolescent↗
PubMed2003

Mycobacteria, an environmental enhancer of lupus nephritis in a mouse model of systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a chronic systemic autoimmune disease characterized by the production of antibodies directed against self antigens. Immune complex glomerulonephritis (GN) is one of the most serious complications of this disorder and can lead to potentially fatal renal failure. The aetiology of SLE is complex and multifactorial, characterized by interacting environmental and genetic factors. Here we examine the nature of the renal pathology in mycobacteria-treated non-obese diabetic (NOD) mice, in order to assess its suitability as a model for studying the aetiopathogenesis of, and possible treatment options for, lupus nephritis (LN) in humans. Both global and segmental proliferative lesions, characterized by increased mesangial matrix and cellularity, were demonstrated on light microscopy, and lesions varied in severity from very mild mesangiopathic GN through to obliteration of capillary lumina and glomerular sclerosis. Mixed isotype immune complexes (IC) consisting of immunoglobulin G (IgG), IgM, IgA and complement C3c were detected using direct immunofluorescence. They were deposited in multiple sites within the glomeruli, as confirmed by electron microscopy. The GN seen in mycobacteria-treated NOD mice therefore strongly resembles the pathology seen in human LN, including mesangiopathic, mesangiocapillary and membranous subclasses of LN. The development of spontaneous mixed isotype IC in the glomeruli of some senescent NOD mice suggests that mycobacterial exposure is accelerating, rather than inducing, the development of GN in this model.

Animals↗
PubMed2002

Some controversies of neuropsychiatric systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is accompanied by several features that can be attributed to involvement of the central or peripheral nervous system. The etiology and pathogenesis of these manifestations are mostly unknown. To which degree these neuropsychiatric conditions can be explained on the basis of chronic illness, or as part of the disease spectrum of SLE, is also a matter of debate. Some of the controversial issues on these matters are discussed in the article.

Fatigue↗
PubMedDate not supplied

An unusual ocular manifestation of discoid lupus erythematosus.

BACKGROUND: Discoid lupus erythematosus is a chronic skin disease characterized by well-demarcated papules and plaques. Mucous membrane changes are common; however, conjunctival involvement is unusual. We report a case of unilateral, chronic, isolated discoid lupus erythematosus of the conjunctiva. OBSERVATIONS: A 32-year-old man presented for evaluation of chronic conjunctivitis of the right eye that had persisted for 9 years. A biopsy of the bulbar conjunctiva revealed a mixed mononuclear cellular infiltrate distributed along the epithelial basement membrane zone and around the stromal blood vessels. Immunohistopathologic examination revealed a diffuse, granular pattern of fluorescence corresponding to immunoglobulins and complement components along the epithelial basement membrane zone and in the walls of the stromal blood vessels. Electron microscopy demonstrated changes in the epithelial basal lamina consistent with discoid lupus erythematosus, including areas that were multilayered. Immunoelectron microscopy identified sub-basal lamina deposits of immunoglobulin G. CONCLUSIONS: Discoid lupus erythematosus should be a suspected cause of chronic conjunctival inflammation; the diagnosis is substantiated by immunopathologic and ultrastructural studies.

Adult↗
PubMed2004

Systemic lupus erythematosus in a multiethnic lupus cohort (LUMINA). XVII. Predictors of self-reported health-related quality of life early in the disease course.

OBJECTIVE: To determine the baseline factors predictive of self-reported health-related quality of life (HRQOL) early in the course of systemic lupus erythematosus patients (SLE) from a multiethnic LUMINA (Lupus in Minorities: Nature versus nurture) cohort. METHODS: LUMINA patients with > or =2 visits were studied. Self-reported HRQOL was examined with the 8 subscales and 2 summary measures (the Physical Component Summary [PCS], and the Mental Component Summary [MCS]) of the Short Form 36 (SF-36). Bivariable and multivariable analyses were done with the PCS, MCS and 8 subscales as the dependent variables. The analyses were performed including and excluding the corresponding SF-36 measure from the independent variables. Age, sex, and ethnicity were included in all models. Time was modeled in all regressions. RESULTS: A total of 1,351 visits (346 patients [80 Hispanics-Texas, 34 Hispanics-Puerto Rico, 126 African Americans, and 106 Caucasians]) were included in these analyses. Mean +/- SD PCS and MCS scores were 36.7 +/- 12.0 and 46.6 +/- 11.5, respectively. The scores for the eight subscales of the SF-36 were also lower than those for the general population. Baseline SF-36 measures were highly predictive of subsequent HRQOL. In the same set of regressions, older age was found to consistently predict poor self-reported HRQOL whereas fibromyalgia, helplessness, fatigue, and abnormal illness-related behaviors were also predictive, but less consistently. Estimated adjusted variances in these regressions ranged from 23% (Role-Emotional [RE]) to 43% (Physical Functioning [PF]). CONCLUSION: In patients with SLE, poor baseline HRQOL was highly predictive of subsequent poor HRQOL. Other predictive variables of poor functioning were primarily psychological/behavioral and socioeconomic-demographic.

Adult↗
PubMed2004

Systemic lupus erythematosus associated with recurrent lupus enteritis and peritonitis.

We describe the case of a 41-year-old woman with systemic lupus erythematosus (SLE) who suffered from repeated reversible lupus enteritis characterized by marked edematous thickening of the small intestine. Ultrasonography (US) and computed tomography (CT) manifested as an 'accordion-like appearance' and a 'target-like appearance', respectively. Resolution of gastrointestinal tract wall thickening was observed on follow-up US performed a week after the increase in predinosolone (PSL). We conclude that careful evaluation of sonographic and radiographic findings helps to establish the diagnosis of lupus enteritis.

Adult↗
PubMed2003

MRI and the brain in systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) can affect any part of the central nervous system (CNS) from the cerebrum to the cauda eqina, giving rise to diverse neurological mainfestations. Despite clinically apparent symptoms and signs, imaging will commonly be normal while at times the magnitude of changes demonstrated on MRI may be out of proportion to the clinical presentation. We describe the MRI techniques used in CNS imaging and the pattern of presentation in SLE.

Brain↗
PubMed2005

Removal of dying cells and systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a very heterogeneous systemic autoimmune disease, in which autoantibody synthesis against nuclear constituents is the main immunological characteristic. These autoantibodies underwent affinity maturation and isotype switching. Additionally, T-cell tolerance against nuclear autoantigens should be affected in these autoimmune patients. Nuclear material derived from apoptotic and/or necrotic cells may serve as an important source of autoantigens. However, dead and dying cells as well as cellular debris are rapidly removed from tissues by phagocytes without eliciting inflammation or immune responses under healthy conditions. During apoptosis nuclear components are strongly modified through enzymatic reactions. If these cells are not timely cleared, those autoantigens may be released, taken up, and presented by dendritic cells in tissues or presented by follicular dendritic cells in lymph nodes to T and B cells, respectively. This could be a mechanism for breaking the peripheral self-tolerance. In this article we focus on the deficient clearance of apoptotic cells in SLE patients and its importance in development of this autoimmune disease.

Journal Article↗
PubMed1995

A Potential Role for PGE and IL-14 (HMW-BCGF) in B-Cell Hyperactivity of Patients with Systemic Lupus Erythematosus.

Systemic lupus erythematosus (SLE) is a disease characterized by the prolonged production of high-affinity autoantibodies resulting in direct and immune complex-mediated tissue damage. Because autoantibody responses occur over several years, memory B cells are likely to be involved. Interleukin-14 (IL-14) is a cytokine implicated in the generation and maintenance of normal memory B cells. Many of the actions of IL-14, including inhibition of antibody synthesis and upregulation of IL-14 receptors (IL-14R), are dependent on the formation of prostaglandin E (PGE) and subsequently cAMP. We observed that IL-14 induces phospholipase A(2) (PLA(2))-dependent release of arachidonic acid from phosphatidylcholine and phosphatidylinositol. Production of PGE is blocked by the PLA(2) inhibitor bromophenacyl bromide. Exogenous PGE (misoprostol) induces similar inhibition of antibody synthesis and increases in IL-14R as IL-14. Lymphocytes from patients with inactive SLE were noted to spontaneously produce PGE. Lymphocytes from normal donors produced PGE only after Sac-activation and IL-14 stimulation. Peripheral B and T lymphocytes from SLE patients, but not normal donors, spontaneously produced IL-14. Increased numbers of peripheral B lymphocytes from patients with inactive SLE expressed IL-14R, when compared to normal donors. Thus, increased production of IL-14 and PGE in SLE may result in expansion of a memory B-cell population capable of long-term autoantibody production. Further study will be necessary to confirm these preliminary findings and to examine in greater depth the regulation of PGE and IL-14 in SLE patients and normal donors.

Journal Article↗
PubMed2004

Health-related quality of life and support group attendance for patients with systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease with variable symptoms. Severity of disease has been associated with mental and physical health-related quality of life (HRQoL). The potential effects of support groups have not been examined. We examined the possible improvement in mental and physical HRQoL of women with SLE who attended support groups. Thirty-four women who attended support groups and 71 comparison women with SLE were recruited. Self-administered surveys included the Medical Outcomes Study Short-Form 36 (SF-36) and a 3-level rating of disease activity.Mean SF-36 Mental Health Summary Scale scores (MCS) were significantly lower for women attending groups (31.5) compared with nonattending SLE women (39.8). MCS scores were lower for blacks compared with whites (33.7 vs. 39.2, P <0.05). Women with high and moderate disease activity had lower MCS scores compared with those with low activity (28.6 or 35.6 vs. 42.7, P <0.05). In linear regression, 27% of the variation in MCS was explained by support group attendance, disease activity, race, and age.Overall, women with SLE reported lower MCS and physical health summary scales (PCS) scores than published population values, indicating markedly reduced quality of life. Any potential positive effects of support groups will need to be tested in a prospective random design to assess improvements in HRQoL.

Journal Article↗
PubMed1993

Elevated serum soluble interleukin-2 receptor levels in subacute cutaneous lupus erythematosus.

Subacute cutaneous lupus erythematosus (SCLE) is a subset of lupus erythematosus which is characterized by unique cutaneous manifestations and immunological abnormalities. Soluble IL-2 receptor (sIL-2 R) is the shed product of membrane Il-2 R, a product of T cell activation. It is measured by enzyme-linked immunosorbent assay (ELISA) and has been found to correlate well with disease activity in systemic lupus erythematosus (SLE) patients. The objective of the present work was to determine whether there is a correlation between sIL-2 R levels and disease activity in SCLE. Serum samples were obtained from 25 SCLE patients and then measured for sIL-2 R levels of ELISA. Fifteen of 25 SCLE patients tested had normal levels of sIL-2 R, while 10 of 25 SCLE patients had elevated sIL-2 R levels. The serum sIL-2 R level in SCLE patients correlated well with disease activity and the number of American College of Rheumatology criteria for SLE. These findings indicate that sIL-2 R levels can be used as a valuable laboratory parameter in managing SCLE patients.

Autoantibodies↗