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At least 721 records · Page 40Linked to original sources
PubMed2005

Increased prevalence of transfusion-transmitted virus and cross-reactivity with immunodominant epitopes of the HRES-1/p28 endogenous retroviral autoantigen in patients with systemic lupus erythematosus.

OBJECTIVE: Systemic lupus erythematosus (SLE) patients produce autoantibodies to HRES-1/p28, a human endogenous retrovirus-encoded nuclear protein. To identify cross-reactive viral antigens capable of triggering autoreactivity, HRES-1/p28 epitopes were mapped by SLE antibodies. METHODS: Forty-four peptides overlapping HRES-1/p28 and 13 viral peptides were synthesized on cellulose membrane and tested for recognition by antibodies from 16 HRES-1 Western blot seropositive SLE patients. Transfusion-transmitted virus (TTV) was detected by gene amplification in sera of 211 SLE patients, 78 healthy SLE family members, 199 unrelated healthy donors, and 91 rheumatoid arthritis (RA) patients. RESULTS: HRES-1/p28 residues 41-55, 121-135, and 156-170 were recognized by 12/16 (75.0%), 11/16 (68.8%), and 9/16 lupus sera (56.25%) and considered immunodominant. HRES-1/p28 residues 121-135 harbor cross-reactive epitope with retroviral peptides and the 70 K U1snRNP lupus autoantigen. HRES-1/p28 residues 41-55 and 156-170 exhibited the highest prevalence of cross-reactivity with TTV peptide ORF2a (14/16, 87%). Prevalence of TTV DNA was increased in lupus patients (120/211) with respect to healthy (66/199; P < 0.0001) or RA controls (23/91; P < 0.0001). TTV prevalence in healthy lupus relatives (40/78) was decreased with respect to lupus patients (80/121; P = 0.0184) and increased with respect to unrelated healthy donors (66/199; P = 0.0026). HRES-1/p28 Western blot reactivity was observed in 12/23 TTV PCR-negative donors and 43/58 TTV PCR-positive donors (P < 0.0281). CONCLUSIONS: Increased prevalence of TTV and molecular mimicry with HRES-1/p28 may contribute to generation of antinuclear antibodies and pathogenesis of SLE.

Adult↗
PubMed2006

Shrinking lungs syndrome, a rare manifestation of systemic lupus erythematosus.

In systemic lupus erythematosus (SLE), the respiratory system is frequently compromised. One of its uncommon manifestations is the shrinking lungs syndrome (SLS), characterised by dyspnoea, diaphragmatic elevation and a restrictive pattern in the spirometry. We report two cases affected with this rare entity. They presented with different degrees of respiratory involvement and responses to the therapy. At the same time, clinical, physiopathological, prognostic and therapeutic aspects of this syndrome are reviewed.

Adult↗
PubMed1985

Decrease in the reaction of DNA repair synthesis in response to nicotinamide or 3-aminobenzamide in ultraviolet irradiated systemic lupus erythematosus lymphocytes.

Systemic lupus erythematosus (SLE) lymphocytes failed to accelerate ultraviolet (UV) induced DNA repair synthesis normally observed following inhibition of poly(adenosine diphosphoribose) polymerization. Without inhibitors of poly(adenosine diphosphoribose) polymerase such as nicotinamide or 3-aminobenzamide, DNA repair synthesis following UV irradiation was found to occur normally in the cells of patients. These data suggest that DNA repair is disturbed under special conditions in the lymphocytes of SLE patients.

Benzamides↗
PubMed1984

Amyloidosis in a case of canine systemic lupus erythematosus.

Concurrent systemic lupus erythematosus (SLE) and amyloidosis (renal and splenic) are reported in a 7-year-old female miniature Schnauzer. Treatment of tissue sections with potassium permanganate and dilute sulphuric acid prior to staining with Congo red indicated that the amyloid in this case is composed of AA protein (i.e. reactive systemic amyloid or so-called secondary amyloid). The rare association of amyloidosis and SLE, in both man and the dog, and the association with granulomatous pneumonia and leukopenia in this case are discussed.

Amyloidosis↗
PubMed1999

[Pregnancy and systemic lupus erythematosus].

Acute disseminated lupus erythematosus primarily affects young women. The highly unfavorable influence of sex hormones is well known and women are advised against pregnancy. Therapeutic termination of pregnancy has been considered necessary. Regular progress in patient management has however completely changed the short, mid and long-term prognosis, although severe forms still resist treatment. As life expectancy improves, better disease control would allow revisiting the possibility of pregnancy. The spontaneous risk of an acute flare-up during pregnancy is debated but estimated in the 60% range. The risk would be about the same whatever the term, but some suggest risk predominates in the third trimester or in the post partum period. The risk of spontaneous abortion is high, partly due to poor disease control and/or the presence of an associated antiphopholipid syndrome. In such cases, preventive therapy (antiaggregates and/or heparin) has greatly improved fetal prognosis. The risk of neonatal lupus (skin eruptions, atrioventricular block) is essentially related to the presence of anti-Ro (SSA) and anti-La (SSB) antibodies. It cannot be well predicted and prevention must be conducted on an individual basis. Overall prognosis of pregnancy can be improved by authorizing pregnancy when the lupus has reached in a well-controlled quiescent phase for at least one year. A multidisciplinary surveillance associating the medical and obstetric teams is required. Preexisting hypertension and renal involvement are unfavorable factors; serum creatinine above 150 mumol/l is considered a contraindication. When good clinical conditions can be achieved, and possibly with low-dose corticosteroids (10 mg/d), the risk of a flare-up is reduced and the rate of fetal survival is almost the same as in the non-lupus female population. The rates of fetal adrenal insufficiency and infection are not significantly higher. Infants are sometimes hypertrophic at birth and are usually born prematurely. Acute pediatric care must be planned. Prognosis in case of "de novo" lupus during pregnancy or pregnancy in a woman with uncontrolled or poorly-controlled lupus remains poor and can be life-threatening for the mother.

Abortion, Spontaneous↗
PubMed1988

Clinical and immunologic effects of monthly administration of intravenous cyclophosphamide in severe systemic lupus erythematosus.

Severe systemic lupus erythematosus affecting the kidney or central nervous system may lead to organ failure or death despite treatment with high doses of corticosteroids. To evaluate the clinical and immunologic effects of intravenous cyclophosphamide in this setting, we treated nine patients with monthly intravenous infusions of cyclophosphamide for six months. A comparison of characteristics at entry and follow-up revealed improvements (by paired t-test) in creatinine clearance (66 vs. 96 ml per minute, P less than 0.001); 24-hour urinary protein level (4.11 vs. 0.90 g, P less than 0.05), Farr anti-DNA titer (43 vs. 8.5 percent, P less than 0.01); complement components C3 (894 vs. 1150 mg per liter, P less than 0.05), C4 (154 vs. 222 mg per liter, P less than 0.05), and total complement activity (CH50) (88.7 vs. 113.4 IU, P less than 0.05); and Westergren erythrocyte sedimentation rate (60.2 vs. 34.4 mm per hour, P less than 0.0005). Other manifestations of lupus improved markedly in most cases, despite a reduction in the mean daily dose of prednisone, from 45 mg at entry to 17 mg at follow-up (P less than 0.01). The numbers of lymphocytes positive for T3, T4, T8, and B1 declined progressively during treatment. At follow-up, persistent decreases were observed in the T-lymphocyte subsets, whereas the absolute number of B lymphocytes had returned to levels near base line. T-cell proliferative responses at follow-up were not significantly different from entry values, except that the response to mitogenic anti-T11 (CD2) antibodies was decreased (P less than 0.01). Our data indicate that monthly intravenous administration of cyclophosphamide was associated with a substantial amelioration of severe systemic lupus, in conjunction with discrete changes in T-lymphocyte markers and T-cell function. This was a preliminary, uncontrolled study, but the results warrant further investigation of this form of treatment.

Adult↗
PubMed1984

[Cytophotometric study of the change in DNA content in the nuclei of human blood lymphocytes in systemic lupus erythematosus].

During systemic lupus erythematosus, a correlation between the nuclear DNA contents in lymphocytes and their tendency to proliferate, on the one hand, and the activity of disease, on the other hand, has been revealed. At the high activity and acute run of disease, a negative tendency of lymphocyte proliferation and negative figures of the index of proliferation prevailed, the findings reflecting the extent of diminution of the lymphocyte DNA amounts. With a decline in the activity of disease and its transition to a phase of remission, a positive proliferative tendency starts to predominate in lymphocytes.

Acute Disease↗
PubMed1986

Current concepts in the etiopathogenesis and treatment of systemic lupus erythematosus (SLE).

Systemic lupus erythematosus is an autoimmune disorder that occurs spontaneously in humans and mice. Genetic factors play an important role in the predisposition to and expression of disease. Environmental factors augment the expression of illness and in the absence of normal control mechanisms may provide the stimulus to autoimmunity. Sex hormones modulate the immune response and tend to modify disease expression. Disordered immune regulation may be due to a primary or secondary abnormality in cellular, cytokine, and/or humoral function. Therapy for SLE is directed towards suppression of exaggerated immunological and inflammatory activity. This review will re-evaluate current therapy and describe newer approaches including the use of pharmacological, hormonal, immunological, dietary, and physical modalities.

Humans↗
PubMed2006

Elevated serum levels of interferon-regulated chemokines are biomarkers for active human systemic lupus erythematosus.

BACKGROUND: Systemic lupus erythematosus (SLE) is a serious systemic autoimmune disorder that affects multiple organ systems and is characterized by unpredictable flares of disease. Recent evidence indicates a role for type I interferon (IFN) in SLE pathogenesis; however, the downstream effects of IFN pathway activation are not well understood. Here we test the hypothesis that type I IFN-regulated proteins are present in the serum of SLE patients and correlate with disease activity. METHODS AND FINDINGS: We performed a comprehensive survey of the serologic proteome in human SLE and identified dysregulated levels of 30 cytokines, chemokines, growth factors, and soluble receptors. Particularly striking was the highly coordinated up-regulation of 12 inflammatory and/or homeostatic chemokines, molecules that direct the movement of leukocytes in the body. Most of the identified chemokines were inducible by type I IFN, and their levels correlated strongly with clinical and laboratory measures of disease activity. CONCLUSIONS: These data suggest that severely disrupted chemokine gradients may contribute to the systemic autoimmunity observed in human SLE. Furthermore, the levels of serum chemokines may serve as convenient biomarkers for disease activity in lupus.

Adult↗
PubMed1992

Transcriptional overexpression of the proto-oncogene bcl-2 in patients with systemic Lupus erythematosus.

In systemic Lupus erythematosus (SLE) spontaneous hyperreactivity of the cells of the immune system leads to the production of pathogenic autoantibodies. A hyperproliferative state of lymphocytes is indicated by the increased expression of nuclear oncogenes. We investigated the expression of a putative proto-oncogene, bcl-2, which is responsible for prolonged survival of lymphocytes and protection from programmed cell death. In 19 of 24 patients with SLE an increased concentration of bcl-2 mRNA was found in unstimulated circulating blood lymphocytes. The overexpression of the bcl-2 gene was more pronounced in patients with active SLE. A pathogenic role of increased bcl-2 expression and prolonged survival of autoimmune memory cells in SLE can be hypothesized.

Adolescent↗
PubMed2002

Initial presentation of hemolytic uremic syndrome in a boy with systemic lupus erythematosus.

Associating systemic lupus erythematosus (SLE) with an initial presentation of hemolytic uremic syndrome (HUS) is rare. We report on a 13-year-old boy admitted to our hospital with an initial complaint of bilateral knee pain and multiple petechiae on both lower extremities. Diagnosis of atypical HUS was established according to the clinical triad of HUS without a veriotoxin-producing organism in his stool and the pathological finding compatible to thrombotic microangiopathy. In addition, his symptoms fulfilled the 1982 revised criteria for the classification of SLE. After methylprednisolone and cyclophosphamide pulse therapies, his laboratory findings and general condition improved. No plasmapheresis or any plasma infusion was required.

Adolescent↗
PubMed1993

Resistance of MHC class I-deficient mice to experimental systemic lupus erythematosus.

Experimental systemic lupus erythematosus (SLE) can be induced in mice by immunization with a human monoclonal antibody to DNA that bears a common idiotype (16/6Id). These mice generate antibodies to 16/6Id, antibodies to DNA, and antibodies directed against nuclear antigens. Subsequently, manifestations of SLE develop, including leukopenia, proteinuria, and immune complex deposits in the kidney. In contrast, after immunization with 16/6Id, mice lacking major histocompatibility complex (MHC) class I molecules generated antibodies to 16/6Id but did not generate antibodies to DNA or to nuclear antigen. Furthermore, they did not develop any of the above clinical manifestations. These results reveal an unexpected function of MHC class I in the induction of autoimmune SLE.

Animals↗
PubMed2005

Pincer nail deformity associated with systemic lupus erythematosus.

BACKGROUND: Systemic lupus erythematosus (SLE) is an autoimmune disorder with various systemic and cutaneous manifestations. Nail abnormalities, including onycholysis, red lunulae, pitting, and ridging, have been seen in patients with the disorder. To our knowledge, however, pincer nail deformity has yet to be reported coincident with the onset of SLE. OBJECTIVE: We report a case of pincer nail deformity subsequent to the development of SLE and describe surgical treatment of the deformed nails. This is followed by a review of the literature. CONCLUSION: Acquired pincer nail is a dystrophy with numerous reported causative associations, including psoriasis, tumors of the nail apparatus, tinea ungium, ss-blocker usage, and now SLE. Pain from the resulting constriction can interfere greatly with daily activities and can be debilitating to the extent of requiring therapy.

Adult↗
PubMed2005

Attempt to correct abnormal signal transduction in T lymphocytes from systemic lupus erythematosus patients.

Systemic lupus erythematosus (SLE) is an autoimmune disease, which predominantly affects females, and causes multiple organ dysfunctions. Recent studies have revealed the underlying immunological abnormalities, especially in lymphocytes from SLE patients. T lymphocytes from SLE patients present abnormalities in T cell receptor (TCR) signaling, for example, decreased expression of TCR zeta chain, PKC theta, and NF-kB p65, decreased PKC dependent protein phosphorylation, impaired translocation of NF-kB p65, decreased production of IL-2 etc. Recently, it is known that reconstitution of deficient TCR zeta chain in T lymphocytes from SLE patients leads to restoration of impaired IL-2 production upon CD3/CD28 stimulation. This time, analysis of abnormal TCR signaling in SLE patients and attempt to correct the impaired IL-2 production by replenishing missing signaling molecules are to be discussed.

Genetic Therapy↗
PubMed1998

Anti-T-cell receptor therapy in murine experimental systemic lupus erythematosus.

Experimental systemic lupus erythematosus (SLE), similar to that observed after immunization with the human anti-DNA mAb 16/6 Id+, could be induced in mice by injection of 16/6 Id specific T-cell lines. The above T-cell lines were exclusively CD4+ CD8- and the majority of cells expressed the Vbeta8 T-cell receptor (TCR) gene products. Furthermore, lymph node cells of mice immunized with the 16/6 Id were enriched with CD4+ Vbeta8+ T-cells. The TCR used by 16/6 Id-specific T-cells showed a limited homology in their CDR3 junctional regions. Nevertheless, mice injected with the anti-Vbeta8 mAb developed autoantibody titers that were not significantly different from those found in the non-treated, 16/6 Id-injected group.

Amino Acid Sequence↗
PubMed1992

Insoluble DNA-like phosphorylated polystyrene: specific interactions with anti-DNA antibodies from systemic lupus erythematosus patients.

Systemic lupus erythematosus (SLE) is an autoimmune disease. Antibodies directed mainly against DNA and/or phospholipids are present in the serum of SLE patients. Therefore phosphorylated polystyrene derivatives acting as DNA-like polymers should be able to interact with the SLE anti-DNA antibodies. Such functional polymers were synthesized and subsequently their interactions with the anti-DNA antibodies studied. Adsorption experiments performed with both anti-DNA antibodies and normal immunoglobulins showed high affinity constants of the phosphorylated polymer for anti-DNA antibodies (4 x 10(9) M-1) whereas for normal IgG the affinity was low (2 x 10(5) M-1). Moreover, the interaction was specific involving the idiotypic moiety of the anti-DNA antibodies and an array of phosphoester groups at the surface of this biomaterial.

Adsorption↗
PubMed1987

Platelet antibodies in systemic lupus erythematosus.

In systemic lupus erythematosus (SLE), the precise cause of the thrombocytopenia is unknown. Since platelet associated IgG is increased in many patients, it has been suggested that the destruction of platelets might be dependent on specific antibodies. In nine patients with SLE, platelet associated immunoglobulins were found together with free serum antibody which bound to platelets from all normal subjects. Using an immunoblotting technique with membrane proteins from normal platelets incubated with patient sera, target antigens were localized on a band of mol wt 108,000 in two cases (B. and N.) and on a band of mol wt 66,000 in a third (M.). When the same technique was applied to autologous platelets of patient N., autoantibody binding to the protein of mol wt 108,000 was demonstrated. The antigenic determinants were not removed from the platelets by enzyme treatment or by disulphide bond reduction, and were localized in the cytoplasmic fraction of the platelets.

Autoantibodies↗
PubMed1989

Circulating colony-forming units of granulocytes and monocytes/macrophages in systemic lupus erythematosus.

In systemic lupus erythematosus (SLE) patients, in vitro bone marrow (BM) colony-forming units of granulocytes and monocytes/macrophages (CFU-GM) are decreased, suggesting that granulomonopoietic failure may play an important role in the mechanism of peripheral blood (PB) depletion of neutrophils and monocytes. No information concerning CFU-GM in PB of patients with SLE is available. The present study was undertaken in order to determine whether SLE itself and the inactive or active stage of disease would modify the number of GFU-GM in PB samples from 20 treatment-free SLE women, 12 inactive and eight active. CFU-GM growth was significantly decreased in both inactive (P = 0.018) and active (P = 0.008) SLE patients as compared with controls (n = 8). The difference in CFU-GM growth between SLE groups was not significant. These results indicate that the number of circulating CFU-GM is significantly reduced in patients with SLE regardless of disease activity or remission.

Female↗