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PubMed1985

Langerhans cells in SLE skin. A role in lymphocyte migration and activation in situ.

Langerhans cells in SLE skin and mucosa were studied by using monoclonal anti-T6 and anti-Ia antibodies and avidin-biotin-peroxidase complex staining. Langerhans cells were present in cell infiltrates of natural SLE skin lesions. In developing early skin lesions induced with test antigen, Langerhans cells were the predominant inflammatory cells, suggesting that migration of Langerhans cells into the inflammatory site in fact precedes lymphocyte migration. These findings agree with the hypothesis of the role of dendritic cells in lymphocyte circulation and antigen presentation under physiological and pathological conditions. Many of the infiltrating local T lymphocytes in both natural and test antigen induced SLE lesions were activated Ia+ cells. This suggests an active immune response in both natural and test antigen induced skin lesions in SLE. The low immunomodulatory T4/T8 ratio in situ in SLE skin lesions might suggest that T8+ cells exert immunosuppressive control on the local inflammation.

Cell Movement↗

PubMed1990

Demonstration of IgE antibodies to nucleic acid antigens in patients with SLE.

Using a combination of avidin-biotin microELISA and solid phase radioimmunoassay, we examined sera from 23 patients with systemic lupus erythematosus (SLE), two patients with established sensitivity to ingested shrimp, and 15 healthy normal subjects. In addition to IgG antibodies, varying amounts of IgE antibodies specific for native DNA (nDNA), denatured or single-stranded DNA (dnDNA), RNA, and tRNA were demonstrable in the sera of SLE patients, but not in the sera of normal subjects. A comparison of the specificity of nucleic acid-specific IgE antibodies present in the sera of shrimp-sensitive patients with those present in the sera of seven SLE patients revealed that the IgE antibodies in the sera of shrimp-sensitive patients specifically recognized shrimp tRNA but not yeast tRNA, calf thymus RNA, or calf thymus DNA, while those present in the sera of patients with SLE recognized all these nucleic acid antigens. The IgE antibodies directed against nDNA, dnDNA, RNA, and tRNA may mediate mast cell and basophil degranulation and thus contribute both to immediate-type hypersensitivity phenomena including hives seen in patients with SLE and to the localization of IgE-nucleic acid complexes in target tissues.

Antibodies, Antinuclear↗

PubMed1990

Relationship between antibodies to dsDNA and to soluble cellular antigens and histologically defined glomerulonephritis in patients with SLE.

To better define the relationships between circulating autoantibodies and renal involvement in systemic lupus erythematosus (SLE), antibodies to both dsDNA and soluble cellular antigens were detected in sera from a large series of SLE patients. Significantly higher dsDNA binding activities and lower complement levels at onset were found in patients with renal disease; however, this was uniquely due to subjects with diffuse or focal proliferative glomerulonephritis. Patients with membranous nephropathy (MGN) showed very low dsDNA binding activities (6/9 of them being negative for dsDNA antibodies) and normal mean C3 and C4 levels. A comparison between patients with proliferative nephritis and patients without renal involvement with high dsDNA binding activities revealed significantly lower complement levels in the former group. No significant difference was observed in the prevalence of antibodies to soluble cellular antigens between patients with or without renal disease; however, nRNP antibody was two-fold more frequent in patients with MGN than in all other subgroups. This study highlights the close relationship between concurrently high anti-dsDNA and low complement levels and proliferative glomerulonephritis in SLE, and suggests that subjects with MGN may represent a subgroup of SLE patients showing peculiar serological features. Different mechanisms possibly involved in the pathogenesis of MGN in SLE are discussed.

Adolescent↗

PubMed1994

Anti-nuclear antibodies associated with schistosomiasis and anti-schistosomal antibodies associated with SLE.

Various autoantibodies to nuclear antigens were detected by ELISA in pooled sera of 15 ICR mice 9 weeks after infection with schistosoma. The binding of this serum with acute infection to cercarial extract was inhibited by prior incubation of the sera with DNA, polynucleotides and cercarial extract. Sera from 9 BALB/c mice with experimentally induced lupus, reacted with cercarial extract. No binding was noted with normal mouse sera (NMS). Similarly, sera of SLE patients (N = 113) reacted with the parasite extracts in a higher incidence (14.2%) compared to NHS (3.7%) (P < 0.05). Immunoblot analysis showed common features to SLE sera reacting with two antigenic "groups". The first are antigens that also were recognized by sera of mice infected with schistosomiasis (60, 85, and 94 kDa cercarial proteins). The second group entailed proteins that bound with SLE sera only (10-18 kDa, 29 kDa and 52 kDa). It can be concluded that antinuclear autoantibodies can be found in sera of acute infected mice with schistosomiasis, while SLE sera may react with 3 schistosomal extracts in a higher incidence than NHS (P < 0.05). These results suggest an autoimmune response in schistosomiasis. It is possible that a parasite infection (as bilharzia) may be one of the "trigger" mechanisms for SLE in a subject with the suitable immunogenetic and hormonal background.

Animals↗

PubMed1999

Abnormal plasma and serum viscosity in systemic lupus erythematosus (SLE): a Jamaican study.

Vascular complications occur frequently in SLE, and their development may be related to haemorheological derangements. However, the range of rheological abnormality in Jamaican SLE patients have not been studied. The present investigation was aimed at determining the changes in the three major blood proteins, namely fibrinogen, albumin and globulin, and their effect on plasma and serum viscosity in SLE patients during the course of treatment. The concentrations of fibrinogen and globulin were significantly increased (p<0.001), while albumin was decreased (p<0.05) in the SLE patients as compared with the control group. This increase in the fibrinogen and globulin contributed significantly to the rise of both serum and plasma viscosity. SLE patients with more severe disease had higher serum viscosity values, suggesting that serum viscosity values may provide an important marker for disease severity.

Adult↗

PubMed2000

Anti-ganglioside antibodies in a large cohort of European patients with systemic lupus erythematosus: clinical, serological, and HLA class II gene associations. European Concerted Action on the Immunogenetics of SLE.

OBJECTIVE: To assay anti-ganglioside antibodies (aGM1) in sera of a large cohort of European patients with systemic lupus erythematosus (SLE) to define the prevalence of these autoantibodies in SLE; to evaluate the association of aGM1 with clinical manifestations and other autoantibodies found in SLE; and to search for aGM1 association with HLA class II alleles. METHODS: Four hundred forty-eight patients with SLE were consecutively enrolled in 8 centers from 6 European countries. All sera were tested for antinuclear antibodies by immunofluorescence on HEp-2 cells as substrate, anti-dsDNA, aGM1, aCL, abeta2-glycoprotein I (abeta2-GPI) antibodies by ELISA, and antineutrophil cytoplasmic antibodies (ANCA) by immunofluorescence and by ELISA. Genomic typing for HLA class II loci was performed by polymerase chain reaction-sequence specific oligonucleotide probe method. Clinical assessment was done at the time of enrolment. RESULTS: We found 41.9% of patients with clinical signs of neuropsychiatric involvement; 15.5% of patients were positive for aGM1, 8% of the IgG isotype and 8.6% of the IgM isotype; aGM1-IgG were associated with neuropsychiatric manifestations (NPM) (RR = 3.7), with migraine (RR = 2.4), with OBS (RR = 7.3), and with peripheral neuropathy (RR = 8.5). aGM1-IgM were associated with NPM (RR = 4) and with depression (RR = 3.4). Furthermore, the genetic study showed that aGM1-IgG were associated with HLA-DQB1*0404 (RR = 7.2) while aGM1-IgM were associated with HLA-DQB1*0605 (RR = 33.3). No associations were found between aGM1 and anti-dsDNA, aCL, abeta2GP1, or ANCA. CONCLUSION: Our results show aGM1 can be found in patients with SLE. aGM1 may play a pathogenetic role for some NPM in this condition.

Adolescent↗

PubMed1976

Immunologic regulation of spontaneous antibodies to DNA and RNA I. Significance of IgM and IgG antibodies in SLE patients and asymptomatic relatives.

Nine individuals from four families of patients with systemic lupus erythematosus (SLE) were studied by sucrose density gradient fractionation and filter radioimmunoassay for the presence of 19S IgM and 7S IgG antibodies to DNA, poly rA, and poly rA-poly rU. One individual in each family was totally asymptomatic, and at least one had actively systemic lupus erythematosus (SLE). The results indicate: (1) a correlation between 7S antibody to DNA and RNA and active SLE, and (2) the presence of 19S antibody to RNA in the asymptomatic relatives. These findings suggest that SLE may be a disorder of immunological regulation. The distribution of antibodies between IgM and IgG is closely related to disease severity. the asymptomatic relatives may have a partial regulatory abnormality resulting in the limited production of IgM antibodies to RNA. SLE patients may have a more complex failure of regulation permitting the additional synthesis of IgG antibodies to DNA and RNA.

Adolescent↗

PubMed2000

[Detection of soluble endothelial protein C receptor (sEPCR) in patients with CHD, DM and SLE].

OBJECTIVE: To evaluate the clinical significance of plasma soluble endothelial protein C receptor (sEPCR) level in patients with coronary heart disease (CHD), diabetes mellitus (DM) and systemic lupus erythematosus (SLE). METHODS: ELISA of antibody-sandwiched principle was used to detect sEPCR in 34 patients with CHD, 42 with DM-II, 63 with SLE and 20 normal controls (NC). RESULTS: The plasma level of sEPCR in patients with DM was higher than that in NC group (P < 0.05). The sEPCR level in SLE patients with thrombosis and non-thrombosis are higher than that in NC group (P < 0.005 and P < 0.001, respectively). There is no significant difference between the two groups of SLE (P > 0.05), and between the CHD and NC groups. CONCLUSION: sEPCR level increased in DM and SLE, it seems related to the process of inflammatory reaction and damage of endothelial cell.

Adolescent↗

PubMed1992

Antibodies against gangliosides in patients with SLE and neurological manifestations.

Pathogenesis of neuropsychiatric manifestations of systemic lupus erythematosus (SLE) has not been clearly defined, and the search for pathogenic mechanisms has focused on the importance of several autoantibodies. There is increasing evidence that antibodies against gangliosides may have a pathogenic role in some neurological disorders. The aim of the present study was to examine the association between antibodies against gangliosides and neuropsychiatric SLE. We found anti-type II ganglioside antibodies in two out of 32 patients with multiple sclerosis (6.25%) and in 10 out of 60 patients with SLE (16.6%); five of 17 patients with neurological abnormalities also had high levels of these antibodies (29.4%). Five of the 10 patients with SLE and positive antiganglioside antibody had only IgM antibodies, three had IgG antibodies and two had both isotypes. By chi-square analysis, the incidence of anti-type II ganglioside antibodies was not significantly higher in patients with symptoms related to the nervous system than in SLE patients without neurological involvement (P > 0.2). No clear correlation was found between antibodies against gangliosides and cardiolipin.

Adolescent↗

PubMed2003

[Analysis of false-positive associated with antibody tests for SARS-CoV in SLE patients].

To discuss the false-positive of serological diagnostic testing for coronavirus antibody in patients with systemic lupus erythematosus(SLE), 66 normal individual and 31 SLE with non-SARS patients were detected for SARS-associated coronavirus (SARS-CoV) antibody and RNA by enzymelinked immunosorbent assays(ELISA) and reverse transcriptase-polymerase chain reaction(RT-PCR). The result showed 2/66 cases(3.0%) were positive of SARS-CoV-IgG antibody and 66 cases were negative of SARS-CoV-IgM antibody in the 66 cases healthy controls; in 31 cases with SLE, positive rates of SARS-CoV-IgG and IgM antibody were 58.1% (18/31) and 29% (9/31), respectively, in which 7 cases(22.6%) were positive of both SARS-CoV-IgG and IgM antibody. All samples of positive SARS-CoV-IgG and IgM antibody were negative by RT-PCR. The ELISA kit coated by non-purification antigen may induce the false-positive of SARS-CoV antibody in patients with SLE. This result suggested that the specificity of ELISA tests for SARS was excellent and has low false-positive rates when using SARS-CoV-IgG and IgM antibody tests. A possible cause of false-positive of SARS-CoV-IgG and IgM antibody in SLE patients is coated antigens with SARS-CoV and Vero-E6 cells in ELISA methods.

Adolescent↗

PubMed2006

IL-1 beta-deficient mice are resistant to induction of experimental SLE.

IL-1 is one of the most pleiotropic pro-inflammatory and immunostimulatory cytokines. Overproduction of IL-1 has been shown to be involved in the pathogenicity of various autoimmune inflammatory diseases, including systemic lupus erythematosus (SLE). However, the different contributions that the IL-1 agonistic molecules make in their in vivo native milieu, IL-1beta which is mainly secreted against IL-1alpha which is mainly cell-associated, have not been established. Experimental SLE can be induced in mice by injection with monoclonal anti-DNA antibodies bearing a major idiotype designated, 16/6Id. In the present study, experimental SLE was induced in mice deficient in specific IL-1 molecules, i.e. IL-1alpha(-/-), IL-1beta(-/-), IL-1alpha/beta(-/-) (double KO) and in control BALB/c mice. Mice deficient in IL-1beta , i.e. IL-1beta(-/-) and IL-1alpha/beta(-/-) mice, developed lower levels of anti-dsDNA antibodies after immunization with 16/6Id, as compared to IL-1alpha(-/-) or control BALB/c mice. Disease manifestations were milder in mice deficient in IL-1beta expression. The representative cytokine cascade that is characteristic of overt experimental SLE was also shown to be reduced in groups of mice that lacked IL-1beta as compared to mice deficient in IL-1alpha, which is mainly cell-associated. Altogether, our results point to the importance of secretable IL-1beta, rather than cell-associated IL-1alpha, in the immunostimulatory and inflammatory phenomena that mediate the pathogenesis of experimental SLE.

Animals↗

PubMed1990

The genetic regulation of the induction of experimental SLE.

We have recently reported the induction of systemic lupus erythematosus (SLE) in C3H.SW female mice by their immunization with a human monoclonal anti-DNA antibody that bears a common idiotype termed 16/6 Id. In the present study, the ability to induce experimental SLE in seven inbred mouse strains by immunization with the 16/6 Id was examined. Two out of the seven strains failed to develop the disease. These two strains did not produce antibodies specific to the 16/6 Id, while the other five strains produced high titres of anti-16/6 Id antibodies. The anti-16/6 Id antibody response, followed by the induction of the disease, was not found to be MHC or Ig heavy chain allotype linked. F1 hybrids between a resistant strain and two of the susceptible strains were found to be resistant to the induction of the disease, indicating that susceptibility is inherited as a recessive trait. In the autoimmune NZB/W F1 female mice, immunization with the 16/6 Id resulted in an early onset of the SLE-like disease. The results of the present study indicate the role of the anti-16/6 Id antibodies in the induction of experimental SLE, and provide direct evidence for the importance of the genetic background in determining susceptibility to SLE.

Animals↗

PubMed1985

Anti-phospholipid antibodies in syphilis and a thrombotic subset of SLE: distinct profiles of epitope specificity.

In a study of connective tissue and infectious disease sera, we have demonstrated IgM and IgG anti-cardiolipin activity, in a solid phase radioimmunoassay, in systemic lupus erythematosus (SLE), rheumatoid arthritis, syphilis and in acute malaria caused by four different species of Plasmodium. The highest values were noted in SLE (IgM anti-cardiolipin P less than 0.005, IgG anti-cardiolipin P less than 0.01), but there was no correlation with anti-dsDNA, rheumatoid factor or VDRL titres in any disease group. Anti-cardiolipin binding was significantly associated with the lupus anticoagulant, thrombocytopenia, spontaneous abortions and thromboses in the SLE patients. Ten SLE sera from this thrombotic subset and 10 syphilitic sera with similar anti-cardiolipin activity, were tested against four phospholipid antigens and showed significantly different anti-phosphatidyl ethanolamine/anti-phosphatidyl serine binding ratios (P less than 0.001). These differences in phospholipid epitope specificity could explain the specificity of the VDRL antigen in syphilis serology, and we discuss a putative role for anti-phosphatidyl serine in the thrombotic diathesis of SLE.

Adult↗

PubMed1987

Differences among immune complexes: association of C1q in SLE immune complexes with renal disease.

Studies that made use of multiple assay systems demonstrated increased levels of immune complexes (IC) in patients with systemic lupus erythematosus (SLE), but no consistent correlations of IC concentration to patterns or activity of disease have been observed. Furthermore, consistent associations between qualitative differences in IC and disease manifestations have been elusive. IC interaction with erythrocytes and mononuclear phagocytic cells is another variable in SLE that may also mediate some of the biological effects of IC. The present report concerns studies of the composition of purified IC obtained from individuals with SLE and other rheumatic diseases; a 64,000 dalton component identified as the A-B subunit of C1q was detected in purified IC from 27 of 51 SLE patients (53%). The presence of this 64,000 dalton component was not related to either IC concentration or to the serum C1q level. However, the presence of the C1q component in isolated SLE IC did correlate with the presence of renal disease (p less than 0.02). These observations are interpreted relative to a recently described kinetic model of IC clearance.

Antigen-Antibody Complex↗

PubMed1987

[Plasma exchange therapy in children and adolescents with systemic lupus erythematosus (SLE)].

Five children (11.5-17.5 years of age) with severe systemic lupus erythematosus (SLE) were treated with plasma exchange. Three children suffered from renal failure and hypertension, one adolescent girl from gastrointestinal and arthritic pains with fever, and one patient from generalized paresis. All patients had excessive serological signs of disease activity. Forty-five sessions of plasma exchange were performed without serious complications. Four children showed improvement of SLE after initiation of plasma exchange in combination with immunosuppressive therapy in two of them renal replacement therapy could be stopped. In the 2 patients with non-renal SLE-complications a dramatic rapid improvement of the symptoms was observed. One girl succumbed to severe hypertension with cerebral bleeding and fungal sepsis after pulsE therapy a few days after start of plasma exchange. Plasma exchange should be started before observation of life threatening complications of SLE. Further information is needed about indication, frequency and duration of plasma exchange in children with SLE.

Adolescent↗

PubMed1985

New lymphokines produced by SLE sera stimulated lymphocytes: the PNAF (polymorphonuclear activating factors).

Twenty-two SLE sera were assessed for their stimulating properties for lymphocytes. After fixation of specific serum factors, lymphocyte cultures were performed and supernatants of 24, 48, 72 and 96 h tested on two polymorphonuclear functions: chemotaxis and cyanide insensitive O2 consumption; 20 out of 22 SLE sera supernatants led to enhanced chemotaxis. The factors involved were not destroyed by heating for 30 min at 56 degrees C. Fifteen of the SLE sera supernatants increased the O2 consumption by PN. In most cases this second mediator was destroyed by heating. The buffer, the normal sera, the monoclonal antibodies stimulated lymphocytes supernatants and the total lymphocyte lysate did not display such enhancing activities. So it clearly appears that SLE sera contain factors acting on lymphocyte membrane and induce them to secrete new lymphokines called PNAF (polymorphonuclear activating factors) which may play a role in pathogenesis of tissue lesions in SLE.

Antilymphocyte Serum↗

PubMed1982

The reaction of human SLE antibodies with native, single stranded RNA: analysis of nucleotide sequence specificities and correlation with Sm and nRNP activities.

The antigenic specificities of RNA reactive IgG autoantibodies from three individual human SLE sera and pooled NZB/NZW mouse serum were studied by competition reactions with synthetic co-polymers and heteropolymers of varying nucleotide compositions. Although minor differences in the individual binding patterns were noted, the RNA reactive immunoglobulins showed a clear preference for G, C and G,C,U containing RNA sequences. All three SLE sera had Sm or RNP activities with rabbit thymus extractable nuclear antigen (ENA). Conversely, all SLE sera that were selected on the basis of their positive ENA reaction could also bind free, single stranded RNA. These results suggest that the autoimmune response to RNA in human and murine SLE is restricted to one or a very few antigenic determinants. They also raise the possibility that autoantibodies to native RNA in SLE sera are partly responsible for ENA reactivity.

Antigen-Antibody Complex↗

PubMed1982

Evidence for an immune complex disorder in systemic lupus erythematosus (SLE).

Immunofluorescence findings have provided evidence for widespread immune complex deposits in SLE. Studies of severe proliferative lupus nephritis have shown that DNA-anti DNA complexes are of major importance. The immune complex systems in the deposits of mesangial and membranous lupus nephritis, as well as in extraglomerular sites have not been thoroughly analyzed, but there is evidence that antinuclear antibodies participate. The key role of DNA complexes in severe lupus nephritis (and probably in other lesions) may be due to its affinity for basement membranes. It is not clear to what extent immune complex deposits are initially formed in situ or as the result of arrest of circulating complexes; in any case, circulating complexes, which are present in high levels in patients with active SLE, are probably of crucial importance in SLE, since they can clearly form deposits in certain sites, add to existing deposits, saturate the reticuloendothelial system and exert other effects, such as on leucocyte function and the immune response. Other pathogenetic mechanisms are also of importance in SLE. In particular, autoantibodies against cell surface antigens can cause abnormalities of circulating cells and possibly parenchymal cells (as shown in studies on anti-brain antibodies). Experimental studies indicate that DTH reactions could account for some of the lesions of SLE, including glomerular lesions, but definitive evaluation of this mechanism awaits the development of techniques that allow positive identification of cell mediated reactions in vivo.

Antibodies, Antinuclear↗