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PubMed1984

Increased photosensitivity to near-ultraviolet light in murine SLE.

We investigated whether there is increased susceptibility to near-UVL in murine SLE. Cultured spleen cells from either strain of mice with lupus disease or conventional strains of mice were exposed to different UVL fractions in vitro. The effect of DNA synthesis, release, and repair was examined. DNA synthesis and release was measured as percent of [3H]thymidine (dT) uptake into either total acid-precipitable radioactive material of cell sediment plus supernatant, or that of the medium alone, whereas hydroxyurea-resistant dT incorporation represented DNA repair. The data indicate that all SLE strains, in contrast to all non-SLE strains, show increased DNA synthesis and release after UV-A exposure. In addition, all murine SLE strains demonstrate increased susceptibility to induction of DNA damage by UV-A. The significance of these observations in relation to the clinical activity of SLE after sunlight exposure is discussed.

Animals↗

PubMed1984

Antibodies to glycosphingolipids in patients with multiple sclerosis and SLE.

We used a liposome lysis assay to measure antibodies against a panel of glycolipids. Antibodies to one or more compounds were detected in 34 of 46 patients with multiple sclerosis, 19 of 31 patients with systemic lupus erythematosus (SLE), and in the majority of patients with cranial trauma or cerebrovascular accidents. Antibodies against ganglioside GM1 and asialo GM1 were found most commonly, and they were frequently present in the same sera. The specificity of the antibodies was tested in four sera that contained antibodies to both glycolipids. The anti-GM1 antibodies cross-reacted with asialo GM1, but the converse was not true. Among patients whose sera contained antibodies to glycolipids, anti-asialo GM1 alone was more common in patients with SLE (7 of 17) than in multiple sclerosis (2 of 34; p = 0.004). Anti-GM1 alone was found in 9 of 34 patients with multiple sclerosis and 1 of 17 patients with SLE, a difference that was not statistically significant (0.135). No correlation was observed between the presence of anti-glycolipid antibodies and symptoms related to the nervous system in patients with SLE. Because of our inability to detect these antibodies by a solid phase immunoassay (ELISA), a comparison was made of the titers obtained with three monoclonal anti-glycolipid antibodies in the liposome lysis assay and ELISA. The ELISA was less sensitive in all instances, requiring from four to 1000 times as much antibody as the liposome lysis assay to give a positive test. We conclude that antibodies to glycolipids occur frequently in patients with multiple sclerosis, SLE, major cranial trauma, and cerebrovascular accidents. Their role in the initiation or perpetuation of inflammatory disease of the central nervous system has yet to be determined.

Antibodies↗

PubMed1982

The clotting defect in SLE.

Haemorrhagic complications, though uncommon in SLE, may be life-threatening in individual patients, and they require treatment along appropriate lines. Thrombotic problems are more commonly encountered, and are a significant cause of morbidity and mortality. Not only is clinical thrombosis important in SLE, but there is increasing evidence that low-grade coagulopathy contributes substantially to many of the pathological features seen in lupus. The mechanisms involved in the pathogenesis of thrombosis have been discussed and their possible interrelationship is summarized in Figure 4, though it remains speculation that low-grade coagulopathy predisposes to clinical thrombosis. Several of these mechanisms may be operating during periods of disease activity; this was suggested in a recent study of clinical and histological features in SLE (Kant et al, 1981). The study was designed to look at the prevalence of glomerular thrombosis in SLE, and its significance as a histological feature. A striking association was observed between the presence of a circulating anticoagulant and the appearance of glomerular thrombosis on renal biopsy. Also, factor VIII levels were significantly increased and circulating platelets decreased in association with "active' histological features. On later re-biopsy glomerulosclerosis was a much more common finding if the first biopsy showed thrombosis, suggesting that thrombosis is a marker of more severe disease activity and inflammation. A greater understanding of the mechanisms promoting thrombosis will undoubtedly provide insight into the pathogenesis of SLE, as well as suggesting new therapeutic possibilities.

Animals↗

PubMed1982

Stimulation of NK-like CMC by skin test antigens in vitro is depressed in patients with SLE.

Peripheral blood mononuclear cells isolated from patients with systemic lupus erythematosus (SLE) developed lower levels of skin test antigen stimulated natural killer cell like cell-mediated cytolysis (NK-like CMC) than did similar cells from age and sex matched non-SLE volunteers. When the subjects were grouped according to disease activity the cells from the patients with mild disease activity developed lower levels of NK-like CMC than did those from the non-SLE control subjects. The cells isolated from SLE patients who had moderate to severely active disease developed little if any NK-like CMC after exposure to various skin test antigens. Greatly decreased skin test antigen stimulation of NK-like CMC in the cells from the SLE patients with more active disease did not appear to be due to therapy with corticosteroids or to a suppressor effect on this response by monocytes present in the peripheral blood mononuclear cell populations.

Adult↗

PubMed1995

[Thrombosis in patients with SLE and antiphospholipid syndrome].

Clinical and serological features in SLE patients with arterial or venous thrombosis were studied. The subjects consisted of 140 patients with SLE who met the revised criteria for the classification of SLE by the American Rheumatism Association. Forty patients (29%) had arterial or venous thrombosis. Arterial thrombosis such as stroke was found in 30 patients, and venous thrombosis such as deep vein thrombosis was seen in 24 patients. Average age at the disease onset was 34.5 +/- 12.5 years old. Renal disorder was found as a clinical feature, and IgG anticardiolipin antibodies (aCL), IgG phospholipid-dependent anti-beta 2-glycoprotein I (beta 2-GPI) antibodies and IgG anti-Annexin V antibodies were identified as serological features in SLE patients with thrombosis. These patients were diagnosed as having antiphospholipid syndrome. It was necessary to perform primary prevention therapy as well as secondary prevention therapy. Multiple thrombotic events in the past history and sustained positive reactions of IgG aCL were suggested as predictors of recurrent thrombosis. These data indicated the clinical and serological characteristics in SLE patients with arterial or venous thrombosis.

Adult↗

PubMed1993

A case complicated with SLE during maintenance hemodialysis.

A 40-year-old woman suffered from toxemia of pregnancy in 1977 and was admitted to hospital. Thereafter, she developed nephrotic syndrome, underwent a renal biopsy, and a diagnosis of membranoproliferative glomerulonephritis (MPGN) was made. She received steroid therapy, immunosuppressive drug and anticoagulant therapy, and recovered sufficiently to be discharged from hospital in April, 1979. During subsequent ambulatory treatment at our outpatient department, her renal function deteriorated gradually, and maintenance hemodialysis was started from June, 1990. In July, 1991, she was admitted to our hospital with pleurisy and pericarditis. There was no improvement despite antibiotic treatments. Laboratory data revealed leukopenia and lymphopenia. Under suspicion of systemic lupus erythematosus (SLE), relevant tests were carried out. Immunological abnormalities such as positive LE cells and the presence of various autoantibodies, together with clinical signs of hypersensitivity to sunlight, stomatitis and serositis, satisfied the diagnostic criteria of the ARA and a diagnosis of SLE was made. This case did not exhibit any clinical or serological abnormalities except for the renal disorder for a 10-year period after the histological diagnosis of MPGN, but was eventually diagnosed as SLE as a result of the manifestation of SLE symptoms for the first time after one year of maintenance hemodialysis. Immunological abnormalities and SLE during maintenance hemodialysis are discussed in relation to other reports.

Adult↗

PubMed1996

[Abnormal Fas and Fas ligand expression of lymphocytes in patients with SLE].

Fas and Fas ligand (FasL) have been assigned a pivotal role for establishment and maintenance of peripheral tolerance of immune system, and mice having defects in Fas/FasL genes develop diseases resembling human systemic lupus erythematosus (SLE). It has been reported that Fas expression of circulating lymphocytes is enhanced in patients with SLE. Nonetheless, apoptosis of SLE lymphocytes is not accelerated. Expression of FasL was detected marginally in unstimulated lymphocytes in normal individuals. In contrast, freshly isolated SLE lymphocytes showed enhanced expression of FasL without in vitro stimulation. We also found the presence of circulating anti-FasL autoantibody in patients with SLE. These results suggest that aberrant FasL expression of lymphocytes and anti-FasL autoantibody are, at least in part, involved in the immune-abnormalities and pathogenesis of the disease.

Animals↗

PubMedDate not supplied

Features of SLE in various ethnic groups in Israel.

OBJECTIVE: To assess the association between the ethnic origin of patients with SLE living in Israel, and the clinical and laboratory features of SLE. METHODS: A retrospective review of medical records was carried out. Patients were classified into 3 groups based on their ethnic origin: a) Ashkenazi Jews, b) Sepharadic Jews and c) Arabs. RESULTS: The study included 74 consecutive SLE patients, 69 (93%) women and 5 (7%) men. Their mean age at diagnosis was 32 years and their mean disease duration was 6.4 years. There were 21 (28%) Ashkenazi Jews, 31 (42%) Sepharadic Jews and 22 (30%) Arabs. The demographics, the frequency of various clinical and laboratory variables of SLE, and the mean disease activity index score (SLEDA1) of the three groups were not statistically different. CONCLUSION: The ethnic origin of SLE patients living in Israel is not associated with the clinical and laboratory features of the disease.

Adult↗

PubMedDate not supplied

HLA-TNF haplotype heterogeneity in Greek SLE patients.

OBJECTIVE: To examine TNF microsatellite allele frequencies in SLE patients in the Greek population, where disease susceptibility is less associated with HLA-DR3 haplotypes. METHODS: A cohort of 46 Greek SLE patients were investigated. Allele frequencies for the TNF microsatellite markers a, b, c and d were determined using a fluorescence based DNA fragment sizing technique. HLA class II typing was performed using a molecular based technique. RESULTS: Associations between SLE and DRB1*1501, *1601 and *0701 were observed and DRB1*0301 was only marginally increased in patients. Linkage disequilibrium was found between DRB1*1501 and TNF a11 and also for DR3 and TNF a2, b3, d2. Stratification of patients suggested that DRB*1501 and TNF a11 frequencies were higher in SLE patients with renal disease and TNF a2 and b 3 frequencies in those without, although these differences did not reach statistical significance. CONCLUSIONS: SLE in this Greek population appears to be associated with a number of HLA-DRB1 alleles. The development of renal complications in these patients may be related to the TNF polymorphism encoded on these HLA haplotypes.

Cohort Studies↗

PubMedDate not supplied

Apoptosis in lupus SLE-N IV and non-lupus mesangiocapillary glomerulonephritis type I MCGN. I. A comparative study.

Apoptosis plays an important role in the recovery from glomerulonephritis. Moreover, aberrant apoptosis seems to contribute to lupus nephritis. This study compared the intensity of apoptosis in lupus and non-lupus mesangiocapillary glomerulonephritis. We used an in situ cell death detection kit, POD, which detects single cell apoptosis in formalin-fixed renal tissue. Our material comprised 13 renal biopsy specimens from patients with lupus mesangiocapillary glomerulonephritis (SLE-N IV), 11 renal tissues from patients with non-lupus mesangiocapillary type I glomerulonephritis (MCGN) and 8 normal kidney samples. We checked the correlations between intraglomerular apoptotic cells and the total number of intraglomerular cells, the relationship between tubulointerstitial apoptotic cells and the relative interstitial cortical volume. The population of intraglomerular apoptotic cells was lower in tissues from SLE-N IV patients than patients with MCGN. In MCGN the intensity of apoptosis in glomeruli correlated significantly with the number of total glomerular cells. Tubulointerstitial apoptotic cells were infrequent in the kidney samples from patients with SLE-N IV and in the normal kidney. In the renal interstitium and tubuli the number of apoptotic cells did not correlate with the relative interstitial cortical volume in kidney tissue in patients with MCGN. In the biopsies from patients with SLE-N IV there was an inverse correlation between tubulointerstitial apoptotic cells and the relative interstitial cortical volume, so a low number of apoptotic tubulointerstitial cells was associated with fibrosis in the renal interstitium. The results illustrate the differences in the intensity of apoptosis in lupus and non-lupus glomerulonephritis. The low number of apoptotic cells in renal tissue from patients with SLE-N IV suggests regulation of apoptosis may be altered in the mechanisms of glomerular and tubulointerstitial damage in lupus nephritis, although the reduced apoptosis may simply be due to smaller numbers of cells in fibrotic areas.

Adult↗

PubMedDate not supplied

Effect of aspirin on liver tests in patients with RA or SLE and in normal volunteers.

Aspirin was given to 20 patients with RA, 16 patients with SLE, and 3 normal volunteers. Four of the RA patients, 7 of the SLE patients, and 1 normal volunteer developed abnormal liver tests, during the study. The abnormalities (elevated transaminases) were most frequent and of rapid onset in patients with cliniclaly active SLE. Increases in BUN and creatinine related to aspirin were observed in several subjects. In a retrospective survey of 80 patients with SLE, aspirin appeared responsible for two-thirds of episodes of liver test abnormalities in 19 patients.

Aspirin↗

PubMed1977

Aseptic necrosis presenting as wrist pain in SLE.

Aseptic necrosis of the wrist in systemic lupus erythematosus (SLE) is not rare. In 156 patients with SLE, aseptic necrosis occurred in 11 patients, of whom 3 (27%) had wrist involvement. Onset of pain was insidious and the symptoms were thought to be related to synovitis due to SLE. An average of 11 months elapsed before aseptic necrosis was correctly diagnosed. An awareness of this possibility is important in the management of any patient with SLE who complains of wrist pain.

Adolescent↗

PubMed2002

Macrosphelide B suppressed metastasis through inhibition of adhesion of sLe(x)/E-selectin molecules.

Macrosphelide B (MSB), a 16-membered macrolide from Microsphaeropsis sp. FO-5050, inhibits adhesion of sialyl Lewis(x) (sLe(x))-expressing HL-60 cells to LPS-activated (E-selectin-expressing) human umbilical vein endothelial cells (HUVECs) in vitro. This study examines MSB effects on metastasis of B16/BL6 mouse melanoma cells (B16/BL6 cells) and L5178Y-ML mouse lymphoma cells in vivo and analyzes the MSB antimetastatic activity mechanism. When administered MSB at 20 mg/kg/day, lung metastatic nodules of B16/BL6 cells were significantly decreased (T/C = 45%). However, no inhibition of metastasis of L5178Y-ML cells to the spleen and liver was observed. Flow cytometry analysis showed that B16/BL6 cells expressed high levels of sLe(x) antigen, whereas expression on L5178Y-ML cells was low. Under in vitro conditions, B16/BL6 cells demonstrated a greater degree of adhesion to LPS-activated HUVECs than L5178Y-ML cells, but adhesion was significantly inhibited by MSB and sLe(x) antibody. Combined therapy of MSB and cisplatin (CDDP) induced remarkable lung metastasis inhibition without adverse effects of CDDP to the host. All these findings suggest that MSB suppresses lung metastasis of B16/BL6 cells by inhibiting cell adhesion to endothelial cells through the sLe(x) molecule.

Animals↗

PubMed1995

IgM anti-A and D SnRNP proteins and IgM anti-dsDNA are closely associated in SLE sera.

U1RNP and Sm precipitins occur in systemic lupus erythematosus (SLE) and in overlap syndromes, while precipitins to Ro/SSA and La/SSB occur in SLE and its variants as well as Sjögren's syndrome. In studying IgM and IgG antibodies to these polypeptides by Western blot, we found the expected frequency of antibodies to the A protein of the U1RNP specificity and the D protein of the Sm specificity in sera with precipitins to U1RNP and Sm, but also found the frequent occurrence of both IgM and IgG anti-A and D in SLE sera with no precipitins, and in sera with anti-Ro/SSA and/or anti-La/SSB precipitins, but not in sera from patients with rheumatoid arthritis, polymyositis, scleroderma, or normals. We have studied the sera which bind the A and D polypeptides on Western blot to test their ability to bind native U1RNP (which contain the A and D proteins) in ELISA. The results indicate that most anti-Ro/SSA alone, anti-Ro/SSA, and anti-La/SSB sera as well as SLE sera with no precipitins react preferentially with the denatured A and D proteins. Further study of sera with IgM anti-A and D in Western blot reveals that these sera also frequently contain anti-double-stranded DNA antibodies. These results show that the anti-A and D responses, especially IgM anti-A and D, occur not only in patients with precipitating antibodies to SnRNPs, but in almost half of patients across the lupus spectrum. The extended prevalence of antibodies to the denatured A and D proteins in Western blot is associated with the cross-reaction of antibodies to dsDNA.

Autoantibodies↗

PubMed1995

IgG anti-F(ab')2 antibodies from SLE patients react with immunodominant residues in kappa CDRs, but show reduced C kappa region reactivity.

We studied reactivity of affinity-purified human IgG anti-F(ab')2 antibodies for antigenic determinants on kappa light chains. Variable (VL) and constant (CL) regions of a human kappa I light chain (EU) were studied for enzyme-linked immunosorbent assay reactivity with monoclonal anti-k antibodies and human IgG antiF(ab')2 using overlapping heptamers of primary sequence synthesized as peptides on polypropylene pins. Polyclonal IgG anti-F(ab')2 antibodies isolated by affinity chromatography from the serum of patients with systemic lupus erythematosus (SLE) were found to react primarily with CDR1- and CDR3-related peptides. The most reactive residues included IL29, TRY32, LEU33, ALA34, GLU90, TYR91, and ASN 92. No striking difference in overall V-region anti-F(ab')2 reactivity profiles was noted when 10 IgG anti-F(ab')2 preparations from normal subjects and SLE patients were compared. In contrast, however, when tested against overlapping C kappa heptamer sequences, the reactivity in SLE-associated anti-F(ab')2 antibodies was markedly decreased. We report that this difference may reflect a defect in anti-idiotypic control mechanisms in SLE.

Amino Acid Sequence↗

PubMed1998

Impaired production of IL-12 in system lupus erythematosus. II: IL-12 production in vitro is correlated negatively with serum IL-10, positively with serum IFN-gamma and negatively with disease activity in SLE.

Interleukin 12 (IL-12) is a key cytokine in regulating type 1 or type 2 cytokine production and in determining the nature of immune responses. Our previous studies demonstrated that its production was significantly impaired in systemic lupus erythematosus (SLE) patients and this deficient IL-12 production was mainly mediated by excessive endogenous IL-10. The present study was designed to further reveal the relationships of in vitro IL-12 production with abnormalities of in vivo cytokine synthesis and disease activity in SLE. Experimental results showed that IL-12 production in vitro was inversely correlated with serum IL-10 level, anti-ds DNA antibody level and SLE disease activity index (DAI), but positively correlated with serum interferon gamma (IFN-gamma) level, with which serum IL-10 correlated negatively. Data also showed that serum IL-10 was significantly higher than that of controls and closely correlated with anti-ds DNA antibody level and SLEDAI. The study confirms that deficient IL-12 production in SLE patients is associated with in vivo abnormalities of cytokine production, especially with increased IL-10 production.

Adult↗

PubMed1997

Correlation between anti-C1q and immune conglutinin levels, but not between levels of antibodies to the structurally related autoantigens C1q and type II collagen in SLE or RA.

The simultaneous appearance of autoantibodies with either a functional or structural relationship to anti-C1q antibodies (anti-C1q) was investigated in 39 systemic lupus erythematosus (SLE) patients and in 28 rheumatoid arthritis (RA) patients, in both cross-sectional and longitudinal design. Levels of anti-C1q showed an isotype-specific correlation to levels of immune con-glutinin (IK) in SLE patients, whereas no correlation was evident to levels of antibodies to the structurally related antigen type II collagen (anti-CII) in SLE or RA patients. IgG anti-C1q levels correlated with serum levels of the terminal complement complex (sC5b-9) in SLE patients. In two longi-tudinally followed patients, the IK response preceded the anti-C1q response. Possibilities for regulation of the humoral anti-complement response are discussed.

Adolescent↗

PubMed1998

Peripheral blood lymphocytes in SLE--hyperexpression of CD154 on T and B lymphocytes and increased number of double negative T cells.

Abnormalities in the regulation of both cell-mediated and humoral immunity have been implicated in the pathophysiology of systemic lupus erythematosus (SLE). Cognate contact-dependent T-B cell interactions involving CD154 (CD40 ligand) on activated T cells and CD40 on B lymphocytes have a critical role in antibody production. Abnormal CD154 expression on lymphocytes may play a role in the production of potentially pathogenic autoantibodies and defects in self-tolerance mechanisms may be important. Failure of intrathymic or peripheral deletion of autoreactive T cells may also result in an autoimmune phenotype. Elevated levels of CD3(+)CD4(-)/8(-) (double negative) T cells (DNT) in the peripheral blood are a surrogate marker for defects of this type. The expression of CD154 on T and B cells was evaluated and levels of double negative T cells in the peripheral blood were assessed by two and three colour flow cytometric analyses. We studied peripheral blood lymphocytes in 48 patients with SLE. Twenty-five normal subjects and 12 patients with rheumatoid arthritis (RA) were studied as disease controls. T cells in 22/48 (45%) lupus patients expressed CD154 between 20-80% (median=52%). In normal controls and RA patients 8-18% T cells were CD154(+). Twelve patients (30%) had elevated expression of CD154 (20-50%) on B cells. In the control RA patients, less than 15% T cells were CD154(+). Twelve of 48 SLE patients had elevated numbers of DNT cells (18-27%). The control subjects had DNT cell numbers <10. These observations suggest that defects in either the intrathymic or peripheral deletion of potentially pathogenic T lymphocytes may play a role in the pathogenesis of SLE. The high expression of CD154 on both T and B cells may also be important in mediating the production of potentially harmful autoantibodies.

Adult↗