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PubMed1995

Complement receptor expression and activation of the complement cascade on B lymphocytes from patients with systemic lupus erythematosus (SLE).

It has previously been reported that the expression of the complement receptors, CR1 on erythrocytes and blood leucocytes and CR2 on B cells, is reduced in patients with SLE, and that the reduced expression of CR1 on erythrocytes is related to disease activity. We have earlier demonstrated that normal B cells are capable of activating the alternative pathway (AP) of complement in a CR2-dependent fashion. In this study we have investigated whether disturbances in this activity may be related to the altered phenotype of SLE B cells. Flow cytometry was used to measure expression of complement receptors and regulatory proteins on B cells from SLE patients, as well as the deposition of C3 fragments occurring in vivo or after in vitro AP activation. We have confirmed, for a proportion of the patients studied, reduced expression of CR1 and CR2 on B cells, and shown a consistency between low CR2 expression and reduced in vitro AP activation in the presence of homologous, normal serum. In addition, the B cells, like erythrocytes, bear raised levels of in vivo-deposited C3dg, but not C3b fragments, compared with normal B cells. The erythrocytes from SLE patients were unable to inhibit in vitro AP activation by B cells in homologous serum. Finally, we demonstrated an inverse relationship between SLE disease activity index (SLEDAI) and the expression of complement receptor 2 (CR2) on SLE B cells. Thus, determination of CR2 on B cells may emerge as an additional laboratory tool in the assessment of SLE activity.

Adult↗

PubMed2005

SLE, atherosclerosis and cardiovascular disease.

Atherosclerosis is an inflammatory disease and the major cause of cardiovascular disease (CVD) in general. Atherosclerotic plaques are characterized by the presence of activated immune competent cells, but antigens and underlying mechanisms causing this immune activation are not well defined. During recent years and with improved treatment of acute disease manifestations, it has become clear that the risk of CVD is very high in a prototypic autoimmune disease, systemic lupus erythematosus (SLE). SLE-related CVD and atherosclerosis are important clinical problems but may in addition also shed light on how immune reactions are related to premature atherosclerosis and atherothrombosis. A combination of traditional and nontraditional risk factors, including dyslipidaemia (and to a varying degree hypertension, diabetes and smoking), inflammation, antiphospholipid antibodies (aPL) and lipid oxidation are related to CVD in SLE. Premature atherosclerosis in some form leading to atherothrombosis is likely to be a major underlying mechanism, though distinctive features if any, of SLE-related atherosclerosis when compared with 'normal' atherosclerosis are not clear. One interesting possibility is that factors such as inflammation or aPL make atherosclerotic lesions in autoimmune disease more prone to rupture than in 'normal' atherosclerosis. Whether premature atherosclerosis is a general feature of SLE or only affects a subgroup of patients remains to be demonstrated. Treatment of SLE patients should also include a close monitoring of traditional risk factors for CVD. In addition, attention should also be paid to nontraditional risk factors such as inflammation and SLE-related factors such as aPL. Hopefully novel therapeutic principles will be developed that target the causes of the inflammation and immune reactions present in atherosclerotic lesions.

Adrenal Cortex Hormones↗

PubMed1986

Decreased expression of C3b receptor (CR1) on erythrocytes of patients with systemic lupus erythematosus contrasts with its normal expression in other systemic diseases and does not correlate with the occurrence or severity of SLE nephritis.

Expression of the C3b/C4b receptor (CR1) on erythrocytes is decreased in patients with systemic lupus erythematosus (SLE) compared to normal individuals, and the CR1 antigen is absent from podocytes in severe diffuse proliferate nephritis of SLE. In the present study, we examined the relationship between the number of CR1 on erythrocytes and the occurrence and severity of SLE nephritis, and assessed the expression of CR1 on erythrocytes and the occurrence and severity of SLE nephritis, and assessed the expression of CR1 on erythrocytes in non-SLE nephritis and other systemic inflammatory diseases by measuring the binding of 125I-labeled rabbit F(ab')2 and murine monoclonal IgG anti-CR1 antibodies to erythrocytes of normal individuals and patients in a French population. The number of binding sites for monoclonal anti-CR1 antibody on erythrocytes of 116 normal individuals was 743 +/- 22 (mean +/- SEM) with a range of 169-1,333, and the frequency distribution of this number in the population was bimodal. In 112 patients with SLE, the mean number of CR1 sites on erythrocytes was decreased to 62% of the mean for normal individuals (p less than 0.001). No correlation was found between CR1 expression on erythrocytes and the presence or immunohistopathological type of glomerulonephritis in biopsy specimens from these patients. The mean number of CR1 on erythrocytes of 29 patients with non-SLE glomerulonephritis was slightly decreased to 89% of the normal mean (p greater than 0.05), which could not be attributed to glomerular immune complex disease or vasculitis.(ABSTRACT TRUNCATED AT 250 WORDS)

Arthritis, Rheumatoid↗

PubMed2001

Indole-3-carbinol in women with SLE: effect on estrogen metabolism and disease activity.

Estrogen metabolism in women with SLE is weighted towards 16alpha-hydroxyestrone, an estrogenic compound that might fuel disease activity. Indole-3-carbinol (I3C) is a nutritional compound that can shift estrogen metabolism towards less estrogenic metabolites. However, the effects of I3C in women with SLE have not been studied. Open-label 1-week metabolic study of 375 mg/day I3C was carried out in women with SLE, followed by a 3-month observational period for disease activity. The primary outcome measure was the change in ratio of urinary 2:16alpha hydroxyestrone levels. Secondary measures included the SLE Disease Activity Index. Seventeen clinically premenopausal women fulfilling ACR criteria for probable/definite SLE (mean age 37.9 y, range 20-49 y, mean disease duration 4.3 y, range 0.5-15) completed the 1-week metabolic study; 12 took I3C for 3 months. The mean 2:16alpha hydroxyestrone ratio increased by 1.84 to 3.15 (P = 0.0001). Mean SLEDAI scores were 10.0 (baseline); 6.25 (3 months); and 8.8 (3 months after withdrawal; P = NS). Women with SLE can manifest a metabolic response to I3C and might benefit from its antiestrogenic effects. We did not observe any striking effects on SLE disease activity during the 3-month observational period.

Adult↗

PubMed1994

Avascular osteonecrosis in patients with SLE: relation to corticosteroid therapy and anticardiolipin antibodies.

Sixty-nine unselected SLE patients were studied to evaluate the prevalence of avascular osteonecrosis (AVN) and its relationship with steroid therapy and with anticardiolipin antibodies (aCL). All the patients were under treatment with corticosteroids. AVN occurred in seven occurred in seven of the 69 patients (10.14%) and was not related to corticosteroid intake. Seventeen of the 69 patients were also treated with methylprednisolone pulse therapy (MPPT) and cumulated the highest corticosteroid doses but none of them suffered from AVN. Excluding the 17 MPPT-treated SLE patients, corticosteroid intake was significantly higher in the AVN-SLE patients. Abnormal IgG and/or IgM aCL serum levels were found in two of the seven AVN-SLE patients and in 24 of the 62 non-AVN SLE, without a statistically significant difference. None of the seven AVN-SLE patients showed features of antiphospholipid syndrome. We conclude that in SLE patients a continuous high-dose steroid treatment may be considered a risk factor for AVN. On the contrary, MPPT regimen may reduce this risk. Anticardiolipin antibodies might represent an added factor which could play a role in some patients but not in all.

Adolescent↗

PubMed1997

Detection of restricted junctional diversity of peripheral T cells in SLE patients by spectratyping.

Analysis of somatic mutations revealed that anti-double-stranded DNA (dsDNA) autoantibodies from patients with systemic lupus erythematosus (SLE) share features of a T cell dependent, antigen driven immune response. Therefore we analysed the length diversity of the complementarity determining region 3 (CDR3) of T cell receptor (TCR) by high resolution gel electrophoresis of 16 V beta family specific RT PCR products (spectratyping). To enable statistical analysis we developed a quantitative scoring method for the histograms. We investigated 16 V beta gene families in peripheral T cells of SLE patients (n = 9) with active (n = 5) and inactive (n = 4) disease as well as normal healthy blood donors (NHD; n = 9). Analysis of TCR V beta spectratypes (active SLE, n = 59; inactive SLE, n = 51 and NHD n = 97) revealed statistically significant differences of CDR3 length distribution between SLE patients and NHD (P < 0.0001 (active SLE/NHD) and P = 0.0034 (inactive SLE/NHD). These results suggest that spectratyping is able to detect clonal activation of peripheral T cells which correlates to disease activity in SLE patients. We conclude that peripheral T cells from SLE patients display features of a secondary antigen driven immune response.

Adolescent↗

PubMed2000

The Leiden mutation of coagulation factor V in Hungarian SLE patients.

We studied the prevalence and the effect of coagulation factor V Leiden mutation on the occurrence of thrombotic episodes in 120 Hungarian patients having systemic lupus erythematosus (SLE) with or without antiphospholipid antibody. The frequency of the factor V Leiden mutation in Hungarian SLE patients was 13%, which is comparable with those found previously in a healthy Caucasian population. The incidence of venous thrombosis among factor V Leiden carriers has been found to be higher (odds ratio [OR] 1.7) than it is in patients without Leiden mutation (38% vs 29%). In addition, the frequency of venous thrombosis in the heterozygous SLE patients (OR 8.4 [confidence interval (CI) 0.8-83.9] P = 0.06) is dependent on the coexistence of other risk factors, such as antiphospholipid antibody. Moreover, among heterozygous factor V SLE patients, the Leiden mutation could explain the tendency to have significantly higher prevalence of fetal losses (OR 3.9 [CI 1.2-12.0] P = 0.02) and higher prevalence of cerebrovascular lesions, cardiac valvular abnormalities, and Raynaud's syndrome than that found in individuals without factor V Leiden mutation of those having antiphospholipid antibody. Systemic lupus erythematosus patients with combined defects suffer more severely from thrombosis than those with a single risk factor do, suggesting that thrombophilia is a multifactorial disorder in SLE, also. Although, the factor V Leiden mutation does not seem to be a significant risk factor for venous thrombosis in SLE, these data demonstrate that Leiden mutation can be regarded as an additive thrombogenic factor providing higher predisposition to several vasoocclusive disorders in SLE.

Abortion, Spontaneous↗

PubMed2006

Cytokine polymorphisms influence treatment outcomes in SLE patients treated with antimalarial drugs.

Antimalarial agents have been widely used as disease-modifying antirheumatic drugs in the treatment of systemic lupus erythematosus (SLE) and other rheumatological diseases, although their mechanism of action has not yet been fully defined. It is known, however, that effective response to treatment is variable among patients. Thus, the identification of genetic predictors of treatment response would provide valuable information for therapeutic intervention. The aim of the present study was to analyze the effect of antimalarial treatment on tumor necrosis factor (TNF)alpha serum levels and evaluate the possible influence of TNFalpha and IL-10 functional genetic polymorphisms on the response to antimalarial drugs. To this end, TNFalpha serum levels were quantified in 171 SLE patients and 215 healthy controls by ELISA techniques and polymorphisms at positions -1,082 and -308 of the IL-10 and TNFalpha gene promoters were determined by PCR amplification followed by hybridization with fluorescent-labeled allele-specific probes in 192 SLE patients and 343 matched controls. Data were related to clinical features and treatment at the time of sampling and during the course of the disease. Results showed a significantly higher amount of serum TNFalpha in the entire SLE population compared with controls. However, TNFalpha serum levels correlated negatively with the use of antimalarial treatment during at least three months before sampling. Patients under single or combined treatment with these drugs had TNFalpha serum levels similar to healthy controls, whereas untreated patients and those under corticosteroid or immunosuppressive therapies had increased amounts of this cytokine. This suggests, however, that antimalarial-mediated inhibition of TNFalpha was only significant in patients who were genetically high TNFalpha or low IL-10 producers. In addition, evaluation of SLE patients administered antimalarial drugs for three or more years who did not require any other specific SLE treatment indicates that patients with the combined genotype low IL-10/high TNFalpha are the best responders to antimalarial therapy, developing mild disease with a good course under this treatment. In conclusion, we proposed that an antimalarial-mediated downregulation of TNFalpha levels in SLE patients is influenced by polymorphisms at IL-10 and TNFalpha promoters. Our results may thus find important clinical application through the identification of patients who are the most likely to benefit from antimalarial therapy.

Adult↗

PubMed1980

Platelet survival and platelet production in systemic lupus erythematosus (SLE).

Platelet survival studies were carried out on 36 patients suffering from SLE. Twelve of them received no therapy, 17 were on corticosteroids (CS), and the remaining 7 received CS and azathioprin (AT). Ten healthy hospital employees served as controls. Only 1 of our SLE patients had thrombocytopenia (platelet count 42 x 10(9)/l). All the remaining 35 patients had venous platelet counts greater than or equal to 120 x 10(9)l. In the control group the average platelet mean life-span (MLS) was 5.8 +/- 0.3 (range 4.0-6.8) days. In the group of untreated SLE patients 3 out of 12 subjects (25%) had a platelet MLS below the lower range for the controls. The mean platelet MLS in the control group did not differ statistically from any of the means of the three groups of SLE patients studied. The lowest mean for platelet MLS (5.2 +/- 0.6 days) was encountered in the group of patients who received no therapy. The means for platelet MLS in the two groups of SLE patients who received immunosuppressive therapy were higher (6.5 +/- 0.4 and 6.6 +/- 0.4 days, respectively) but did not differ statistically from the mean of untreated patients (0.10 > p > 0.05). The mean platelet production rate in the control group (23 +/- 10(10) platelets per day) did not differ from any of the three groups of SLE patients investigated. In the literature it has been proposed that a state of compensated thrombocytolysis is present in most cases of SLE. The results of the present study do not support this hypothesis, however.

Adrenal Cortex Hormones↗

PubMed1998

[The association of sasceptibility of SLE and the gene polymorphism of TNF].

OBJECTIVE: To evaluate the association between the susceptibility of SLE and the gene polymorphism of TNF in Chinese Han population. METHODS: The single base change polymorphism in both TNF alpha gene and TNF beta gene were analyzed among SLE patients and normal controls by using PCR-SSCP and PCR-RFLP. RESULTS: No difference of gene or genotype frequencies of TNF alpha was noted in SLE patients and normal controls (P > 0.5), whereas TNF beta * 2 gene frequency increased significantly in SLE patients (SLE patients 65.7%, normal people 54.5%, P < 0.05). CONCLUSION: TNF alpha gene polymorphism has no effect on SLE, but TNF beta * 2 allelic type may be related to the susceptibility of SLE in Chinese Han population to some extent.

Adolescent↗

PubMedDate not supplied

Autoantibodies to alpha-fodrin in primary Sjögren's syndrome and SLE detected by an in vitro transcription and translation assay.

OBJECTIVE: To investigate the prevalence of alpha-fodrin autoantibodies in primary Sjögren's syndrome (SS) and systemic lupus erythematosus (SLE) with and without secondary SS, using an in vitro transcription and translation assay (ITT). METHODS: cDNA encoding JS-1, the amino-terminal portion of alpha-fodrin, was used for ITT. Immunoprecipitation was performed with sera from 56 primary SS patients and 67 SLE patients, 14 with and 53 without secondary SS. Correlations to RF, ANA, anti-dsDNA, anti-SS-A and anti-SS-B antibodies, hypergammaglobulinemia, labial salivary gland biopsy grade, extraglandular manifestations and a modified SLE disease activity index (mSLEDAI) were made. RESULTS: Autoantibodies against alpha-fodrin were detected in 16/56 (29%) of primary SS patients and in 25/53 (47%) of sera from SLE patients without secondary SS. In SLE patients with secondary SS the prevalence was 3/14 (21%). None of the blood donors showed alpha-fodrin reactivity. Correlations were found to RF, ANA, anti-dsDNA antibodies and a positive mSLEDAI score. CONCLUSION: The frequency of alpha-fodrin autoantibodies detected by this method is similar in sera from primary SS patients and SLE patients with or without secondary SS. The presence of alpha-fodrin autoantibodies seems to reflect non-organ-specific autoimmunity in primary SS and SLE and to be of limited discriminating value.

Autoantibodies↗

PubMed2003

Increased estrogen-dependent expression of calcineurin in female SLE T cells is regulated by multiple mechanisms.

OBJECTIVE: Calcineurin is a key mediator of T cell activation. Previous studies in our laboratory showed a dose-dependent and hormone-specific increase in calcineurin expression in the T cells from females with systemic lupus erythematosus (SLE). This study investigates whether the estrogen-dependent increase in calcineurin expression is due to stabilization of the messenger RNA (mRNA). METHODS: T cells from female patients with SLE and controls were cultured for 18 hours in a serum-free medium with and without estradiol-17 beta (10(-7) M). Some T cells were activated by further culture on anti-CD3-coated plates. Actinomycin D (25 micrograms/mL) was added to some cultures to inhibit new mRNA synthesis. Calcineurin mRNA stability was assessed by reverse-transcription polymerase chain amplification. RESULTS: Resting SLE (n = 9, P = .59) and normal (n = 5, P = .90) T cells showed no significant differences in mRNA stability in response to estradiol. Calcineurin mRNA was not significantly stabilized in activated SLE (n = 10, P = .12) or activated normal (n = 8, P = .09) T cells in response to estradiol. However, the amount of calcineurin mRNA stabilized in activated normal T cells (n = 8) was significantly greater (P = .02) compared with SLE T cells (n = 10) only after culture in medium without estradiol. CONCLUSIONS: These findings highlight the complex gene regulatory mechanisms underlying the differential action of estrogen on SLE T cells. Furthermore, the data indicate that increased calcineurin expression in SLE T cells is not due solely to estrogen-dependent stabilization of the message, and probably involves additional transcriptional regulatory mechanisms.

Adult↗

PubMedDate not supplied

[Migraine in SLE: role of antiphospholipid antibodies and Raynaud's phenomenon].

OBJECTIVES: To determine the role of antiphospholipid antibodies (aPL) and of Raynaud's phenomenon (RP) in the development of migraine in patients with systemic lupus erythematosus (SLE). METHODS: 50 unselected SLE patients and 20 rheumatoid arthritis (RA) controls underwent an interview to define the presence of migraine according to the guidelines of the International Headache Society (1988). Serological tests for aPL were performed in all patients. SLE patients were divided according to positivity for RP and/or aPL into 4 subsets: R-/aPL-, R-/aPL+, R+/aPL- and R+/aPL+. Data were analysed using Fisher's exact test, Chi-square test and U Mann-Whitney test. RESULTS: SLE and RA patients were similar for demographic and clinical features; aPL positivity was found in a greater proportion of SLE patients versus RA controls (68% vs 25%, p=0.0036). 31 of the 50 lupic patients (62%) and 7 of the 20 RA controls (35%) suffered from migraine (OR=3, CI:1-8.9). Among SLE and RA patients, migraine was associated with aPL positivity (p=0.027 and p=0.019). Analysing the combined effect of aPL and RP on migraine, in R+/aPL+ patients we detected an higher frequency of migraine (85.7%) with respect to the patients negative for these two features (27%, p=0.0051, OR=16, CI:2.2-118) and to the patients positive only for aPL (65%, p=0.0031, OR=6.2, CI:1.2-32). CONCLUSIONS: Migraine in SLE and RA associates with aPL positivity. The simultaneous presence of RP increases by 2,5 times the probability of having migraine, suggesting that cerebral vasospasm might be more common in patients with peripheral vasospasm, given the presence of aPL.

Adult↗

PubMed2006

[Role of Fas-FasL and caspase-3 signal transduction pathway in promoting apoptosis of T lymphocyte subset in SLE patients].

AIM: To explore the relationship between Fas-FasL-mediated signal transduction pathway and apoptosis disorder of T lymphocyte subset in SLE patients. METHODS: The expression rate of membrane Fas, FasL and that of intracellular activated caspase-3 of T lymphocyte subset were determined by flow cytometry. RESULTS: Compared with healthy control group, the expression rate of membrane Fas on CD4(+) T cells significantly increased in SLE patients in the active and inactive phases (P<0.05), however, that on CD8(+) T cells slightly increased but there was no statistical significance (P>0.05). The expression rate of FasL on T cell subset in SLE patients in the active and inactive phases significantly increased (P<0.05) but there was no obvious difference of the expression rate of Fas and FasL on T cell subset between the two disease groups (P>0.05). The expression rate of intracellular activated caspase-3 in T cell subset of SLE patients in the active phase was notably higher than that in the inactive phase and healthy control group (P<0.05). The expression rate of intracellular activated caspase-3 in T cell subset of SLE patients in the inactive phase was slightly higher than that in health control group but there was no statistical significance. CONCLUSION: Apoptotic speed of T lymphocyte subset in SLE patients was accelerated while CD4(+) T cells were in a state of active apoptosis. It is possible that Fas-FasL signal transduction pathway plays an important role in the induction of T cell apoptosis. The degree of apoptosis of T lymphocytes closely correlates with the disease's activity in SLE patients.

Adolescent↗

PubMedDate not supplied

Restricted specificity of anti-ribosomal P antibodies to SLE patients in Israel.

OBJECTIVE: Anti-ribosomal P antibodies (aRib-P Ab) are highly specific for systemic lupus erythematosus (SLE), but their correlatation with disease activity and manifestations including renal, hepatic and central nervous system (CNS) involvement is still controversial. The aim of our study was to evaluate the prevalence of aRib-P Ab and their correlation with clinical manifestations and anti-dsDNA antibodies in SLE patients from Israel. METHODS: Elevated titers of aRib-P Ab utilizing the ELISA method were analyzed in 141 sera samples from 44 SLE patients, 20 Familial Mediterranean Fever (FMF) patients, 22 primary antiphospholipid syndrome (PAPS) patients, 12 patients with infections, and 43 healthy individuals. The SLEDAI score was utilized for assessing SLE disease activity. RESULTS: Elevated titers of aRib-P Ab were present in 11% of SLE patients (n = 6). The mean SLEDAI was 7 (range: 3-10). No statistically significant association was observed between the presence of aRib-P Ab and disease manifestations present in the SLEDAI. The 6 SLE patients had renal disease (n = 1), leucopenia (n = 1), rash (n = 3), and CNS involvement manifested as psychosis (n = 1) or depression (n = 1). Elevated titers of anti-dsDNA antibodies were found in 50% of patients with elevated titers of aRib- P Ab. Patients with PAPS, FMF, infections or healthy controls did not harbor elevated titers of aRib-P Ab. CONCLUSION: Elevated titers of aRib-P Ab were restricted to SLE patients. We confirm previously reported associations of aRib-P Ab reactivity with disease activity and elevated anti-dsDNA Ab titers. No significant correlation with a specific manifestation described on the SLEDAI score was established in this small cohort of patients.

Adolescent↗

PubMed1986

Analysis of antigen specific T cell helper function in first degree relatives of patients with systemic lupus erythematosus (SLE).

Fourteen families with first degree relatives of patients with systemic lupus erythematosus (SLE) were studied for the ability of their members to respond to the synthetic polypeptide antigen (T,G)-A-L. The family members were also tested for their HLA determinants. All SLE patients tested responded to (T,G)-A-L as measured by the production of (T,G)-A-L specific T cell helper factors by their antigen activated T cells, confirming our previous findings that 100% of SLE donors responded to (T,G)-A-L in contrast to 50% responders in a control population of healthy donors. The general defect in the regulation of immune responses in SLE patients was further indicated by the demonstration that an SLE patient who is a daughter of non-responder parents to (T,G)-A-L, responded to this genetically regulated antigen. In contrast to our observations with SLE patients, the genetic regulation of the ability to respond to (T,G)-A-L was shown not to be impaired in healthy first degree family members of SLE patients and the segregation of the immune response potential in these families was as expected from an inherited dominant trait.

Animals↗

PubMedDate not supplied

In vitro autoantibody synthesis by anti-La(SSB) positive SLE patients and healthy controls.

In vitro production of anti-La(SSB) and anti-DNA antibodies by mononuclear cells (mnc) from systemic lupus erythematosus (SLE) patients and healthy controls was measured using ELISA techniques. The SLE patients were divided into anti-La(SSB) positive and negative groups depending on Ouchterlony analysis of the serum. Both patient groups spontaneously produced raised levels of total IgG but not IgM compared to controls. Pokeweed mitogen (PWM) stimulated mnc from anti-La(SSB) positive SLE patients and controls gave good total IgM and IgG responses. In contrast the anti-La(SSB) negative group gave no IgG but did make an IgM response. Kinetic studies showed that 14 day cultures were essential to produce detectable amounts of specific autoantibodies which, with a few exceptions, were of IgM isotype. Low levels of anti-La(SSB) and anti-DNA were spontaneously produced by anti-La(SSB) positive SLE patients and controls. PWM stimulation at least doubled autoantibody synthesis in these two groups. The anti-La(SSB) negative SLE group gave similar responses although PWM induced autoantibody levels were reduced. ConA-induced suppressor cell assay showed that anti-La(SSB) positive SLE patients could form suppressor cells but not as effectively as controls. This group of SLE patients were more successful at suppressing IgG than IgM responses.

Adult↗

PubMed1984

Auto-anti-anti-DNA antibodies from SLE patients and normals.

Cross reacting auto-anti-idiotypic antibodies against anti-ssDNA antibodies were investigated in patients with systemic lupus erythematosus (SLE) and normals. Sera or immunoglobulins from SLE and normals depleted of anti-ssDNA activity and DNA antigen inhibited the reaction between 125I-F(ab')2 anti-ssDNA and ssDNA. In addition, binding to F(ab')2 portions of chromatographically purified portions of anti-ssDNA coated on polystyrene wells could be measured both in depleted SLE and normal sera. Depleted sera from SLE had both greater inhibitory activity and more antibody binding capacity than depleted sera from normals. IgG from SLE sera bound to both F(ab')2 anti-ssDNA and SLE F(ab')2 non-anti-ssDNA. However, the binding of IgG to F(ab')2 anti-ssDNA was significantly inhibited by ssDNA. These results indicate that cross reacting auto-anti-anti-ssDNA as well as other antibodies to F(ab')2 portions of homologous IgG are found in higher concentration in SLE than in normals.

Antibodies, Anti-Idiotypic↗