SEARCH · PubMed Health

Results for “SLE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 253 records · Page 14Linked to original sources

PubMed2000

Histone-containing immune complexes are to a large extent responsible for anti-dsDNA reactivity in the Farr assay of active SLE patients.

Increased titres of anti-dsDNA antibodies, especially if of high avidity, are associated with renal exacerbations in patients with systemic lupus erythematosus (SLE). One of the most reliable assays to measure anti-dsDNA antibodies, the Farr assay, is believed to detect preferentially high avidity antibodies. Purified non-complexed monoclonal antibodies (mAbs) against nucleosomes, obtained from mice with SLE, are not reactive in the Farr assay, but can become so once complexed to nucleosomes. These Farr-positive, nucleosome containing, immune complexes were also able to bind in vivo to the glomerular basement membrane (GBM), predominantly via heparan sulphate (HS). To evaluate whether in SLE patients the same kind of immune complexes are responsible for Farr reactivity, IgG from serum or plasma was isolated under dissociating and physiological conditions. We observed that after purification under dissociating conditions, Farr reactivity was significantly decreased (P<0.0001) in contrast to reactivity with histones and two 'control' antigens: Epstein Barr Virus (EBV) and Ro/SS-A. Reactivity with nucleosomes also decreased after purification, although to a lesser extent. Plasma purified under physiological conditions showed no decrease in Farr reactivity. The importance of histones for the generation of immune complexes is supported by the two following observations. Firstly, the presence of histones could be demonstrated in serum and plasma of SLE patients but not in serum of healthy controls or in IgG preparations purified under dissociating conditions. Secondly, Farr reactivity of purified IgG preparations could be restored by addition of purified histones. From these studies we conclude that histones containing immune complexes are responsible for a large part of the Farr reactivity in active SLE, and are therefore indirectly implicated in the pathogenesis of lupus nephritis.

Animals↗

PubMed2001

Binding of SLE autoantibodies to native poly(I), ROS-poly(I) and native DNA: a comparative study.

Reactive oxygen species (ROS) are implicated in a variety of human diseases. The formation of pathogenic anti-DNA antibodies in systemic lupus erythematosus (SLE) has been extensively investigated. ROS-modified DNA has been found to be a better antigen for anti-DNA antibodies found in SLE sera. A comparative binding of SLE autoantibodies with native poly(I), ROS-poly(I) and nDNA has been studied. Affinity-purified SLE IgG exhibited a high degree of specificity towards the ROS-modified poly(I) in comparison to native DNA and native poly(I), reiterated visually by gel retardation assay. The data suggested that hydroxyl radical-modified nucleic acids like RNA and DNA might be agent for the induction of circulating SLE anti-DNA autoantibodies.

Antibodies, Antinuclear↗

PubMed1988

Anti-Sm and anti-DNA antibodies in paired serum and synovial fluid samples from patients with SLE.

Antibodies to nuclear antigens (ANAs) are frequently found in the serum of patients with connective tissue diseases (CTDs). Particularly systemic lupus erythematosus (SLE), and have been implicated in the immune-complex mediated pathogenesis of these diseases. In this study we have compared the occurrence of precipitating ANAs in paired samples of serum and synovial fluid from patients with different CTDs. Of the 30 patients examined 3 had precipitating ANAs in their serum only, 1 in the synovial fluid only, and 3 had antibodies in both serum and synovial fluid. Precipitating ANAs in synovial fluid were found in 3/6 patients with SLE, 1 patient with RA/Sjogren's syndrome overlap, and one patient with RA/SLE overlap. Of the other 15 patients with RA, 2 had precipitating antibodies only in their serum. Two of the SLE patients had anti-Sm antibody, one in serum only and the other in both serum and synovial fluid. Detection by ELISA of class specific anti-Sm antibodies in serum or synovial fluid paralleled the occurrence of antidenatured DNA antibodies when both specificities occurred together. One SLE patient did show evidence in synovial fluids of elevated concentrations of specific antibody classes to individual antigens; however, elevated levels were more frequently found in serum. Local production of ANAs does not, therefore, appear to be a feature of synovial fluids from SLE patients.

Antibodies↗

PubMed1983

DNA antibodies and complement in SLE patients. A follow-up study.

Sixty-seven patients with systemic lupus erythematosus (SLE) were followed up for 3-19 months (mean 12) in a prospective study. The activity of SLE was estimated on clinical grounds and correlated with DNA antibody and complement levels. The disease reactivations consisted mostly of articular and cutaneous symptoms. There were 17 relapses and 22 complicating infections during the follow-up period. The levels of antibodies to native, double-stranded (ds) DNA (P less than 0.001) and antibodies to denatured, single-stranded (ss) DNA of IgG class (P less than 0.001) and C3 (P less than 0.001) correlated best with disease activity, which was estimated on the clinical symptoms and signs. These assays were not reliable, however, in predicting minor exacerbations. The levels of IgM class ss-DNA antibodies were significantly higher in SLE patients without nephritis than in SLE nephritis patients. In most cases, the combination of IgG class ss-DNA antibody and complement (C3 and CH50) determinations differentiated SLE relapse from infection.

Autoantibodies↗

PubMed1988

In vitro T-cell functions specific to an anti-DNA idiotype and serological markers in patients with systemic lupus erythematosus (SLE).

The human monoclonal autoantibody 16/6 is a common anti-DNA idiotype found to have clinical relevance in patients with systemic lupus erythematosus (SLE). Therefore the ability of peripheral blood T cells of SLE patients and healthy controls to proliferate and to produce helper T-cell factors following stimulation with this idiotype was tested. It was found that T cells of 75% of healthy donors proliferated to the 16/6 idiotype, whereas only 22% of SLE patients responded to this idiotype by proliferation. On the other hand, the capability to produce T-cell helper factors specific to the 16/6 idiotype was found in a higher percentage of SLE patients (48%) as compared to healthy controls (31%). The low frequency of proliferative responses in SLE patients might be due either to the chronic exposure to the 16/6 idiotype or to the production of antiidiotype antibodies against the 16/6 idiotype, which interfere with the response to the latter stimulator.

Adolescent↗

PubMed1996

Evaluation of the BCL-2 gene locus as a susceptibility locus linked to the clinical expression of systemic lupus erythematosus (SLE).

Systemic lupus erythematosus (SLE) is an autoimmune disease characterised by the production of a large number of autoantibodies. It has been postulated that this may be the result of prolonged longevity of auto-reactive B cells due to defective regulation of programmed cell death (apoptosis). The proto-oncogene bcl-2 is involved in the control of apoptosis in immunocompetent cells, and its over-expression is noted in T and B cells from SLE patients. This study examined the genetic linkage between the bcl-2 gene locus and SLE susceptibility using the affected sib-pair method in SLE families. Seventeen caucasian multiplex families were evaluated. A polymorphic microsatellite marker closely linked to the bcl-2 gene on 18q21.3 was used to determine the bcl-2 genotype. We demonstrated that haplotype sharing among the affected sibling pairs was not statistically different from random (P > 0.5). This suggests that the bcl-2 gene locus does not confer a genetic susceptibility to SLE expression.

Alleles↗

PubMed1986

C-reactive protein (CRP) levels in systemic lupus erythematosus (SLE).

CRP levels in 194 serum samples from 43 SLE patients were measured. Patients with inactive disease have levels below 10 micrograms/ml; patients with active SLE have higher levels, but never over 50 micrograms/ml. In the presence of infection or inflammatory processes, regardless of the activity of SLE, the levels are significantly higher (p less than 0.05), and well over 50 micrograms/ml. Both active SLE patients and inactive SLE patients with local infections have levels between 10 micrograms/ml and 50 micrograms/ml. In this situation, the presence of anti-DNA antibodies strongly suggests disease activity (82% versus 9%, p less than 0.05). The clinical and physiopathological meaning of these findings is discussed.

Antibodies, Antinuclear↗

PubMed1998

Association of IgA anti-dsDNA antibodies with vasculitis and disease activity in systemic lupus erythematosus. SLE Study Group.

Previously it has been suggested that the presence of antibodies against dsDNA of the IgA class may define a subset of systemic lupus erythematosus (SLE) patients suffering from nephritis and arthritis. Therefore, these autoantibodies were measured in sera of 352 patients with SLE, 81 blood donors, and 189 patients with rheumatoid arthritis using a new ELISA based on human recombinant dsDNA as antigen. IgA anti-dsDNA antibodies were found in 19.9% of the sera from patients with SLE, but in none of the sera from 81 normal controls and 189 patients with rheumatoid arthritis. The association of these autoantibodies with 31 clinical and 36 laboratory parameters was calculated. IgA anti-dsDNA antibodies were found to be associated with parameters of disease activity such as elevated erythrocyte sedimentation rate and consumption of complement component C3, and the clinical parameters vasculitis, with necrosis and erythema, but not with nephritis and arthritis. Therefore, IgA anti-dsDNA antibodies define a subset of SLE patients, and monitoring of IgA anti-dsDNA antibodies may be helpful as a prognostic parameter in patients with SLE.

Antibodies, Antinuclear↗

PubMed2004

Immunoadsorption (IAS) as a rescue therapy in SLE: considerations on safety and efficacy.

OBJECTIVE: In SLE, extracorporeal procedures aiming at reduction of immunoglobulin (Ig) and immune complexes (IC) are used as a rescue therapy. Plasma exchange (PE) has not been proven overall effective in SLE, and long-term treatment in particular has been associated with severe bacterial and viral infections. Immunoadsorption (IAS), in contrast, selectively removes Ig and IC and may thus be safer. We therefore investigated the rate of infections in SLE patients who were undergoing long-term IAS. METHODS: 16 SLE patients were treated with > or = 10 courses of IAS, and nine patients with highly active disease received pulse cyclophosphamide (IVCP) therapy in parallel. We retrospectively analysed the records of all these patients for the occurrence of infections. Patients receiving IAS therapy plus IVCP were compared with 25 patients with similarly active disease treated with standard IVCP therapy within the same observation period. Patients receiving IAS without additional IVCP were compared with patients with similarly moderate disease activity receiving neither IAS nor IVCP. RESULTS: No potentially life-threatening viral infection occurred in IAS-treated patients and episodes of herpes zoster were equally distributed. No severe infection was observed during IAS without concomittant cyclophosphamide. As expected, more patients with highly active disease receiving IVCP experienced infections than those with less active disease (16 of 34 [47%] vs. 2 of 22 [9%], p < 0.04). On comparing the two groups with highly active disease, infections were similar (IAS+IVCP: 3 of 9 patients [33%], IVCP only: 5 of 25 [20%]), but one patient receiving IAS+IVCP died of septicaemia. Disease activity significantly decreased in both groups treated with IAS. CONCLUSION: IAS has an acceptable safety profile with regard to severe infections and appears safe with regard to severe viral disease. Highly active disease and IVCP therapy increase the risk of severe infections in SLE.

Adolescent↗

PubMed2005

C1q complement component and -antibodies reflect SLE activity and kidney involvement.

The role of the complement system in the pathogenesis of systemic diseases is very ambivalent. In systemic lupus erythematosus (SLE), many abnormalities in the activation of the complement system have been reported. The most important antibodies formed against the complement system in SLE are the ones associated with the C1q component. The aim of this study was to assess separately the anti-C1q antibodies and C1q component in the serum from 65 patients with SLE, then in individuals with (n=33) and without (n=32) lupus nephritis and with active (n=36) and nonactive (n=29) form of the disease (European Consensus Lupus Activity Measurement, ECLAM>3, ECLAM<or=3). This study also aims to look for correlations with other clinical and laboratory parameters. The C1q antibodies were measured by the Enzyme-Linked Immunosorbent Assay (ELISA) test, while radial immunodiffusion according to Mancini was used to measure the C1q complement component. The mean serum levels were 90.89+/-13 IU/ml for anti-C1q antibodies and 145+/-52 mg/l for C1q. The significant difference in C1q antibodies levels was found between individuals with and without lupus nephritis (117.5+/-52 IU/ml vs. 28.2+/-12.2 IU/ml, p=0.0001) and between those with active and nonactive SLE (154.6+/-115 IU/ml vs. 50.6+/-73, p=0.001). C1q complement component was statistically lower in patients with lupus nephritis (144+/-30 mg/l vs. 175+/-50 mg/ml, p=0.002) and in active patients (138+/-40 mg/l vs. 202+/-20 mg/l, p=0.001). If the two parameters are measured together, they seem to have a mirror-like pattern of serum concentration, and they are potential markers of SLE activity and of the presence of lupus nephritis.

Adolescent↗

PubMed2001

Factors associated with anxiety, depression and suicide ideation in female outpatients with SLE in Japan.

The subjects consisted of 84 female SLE outpatients who were all over 20 years of age. These patients were able to maintain relatively stable physical conditions and lead normal daily lives, and they were regularly treated at the outpatient clinic. All subjects were Japanese. Psychological features (trait anxiety, state anxiety, depression and suicide ideation) were evaluated using psychological tests, and the relationships between the respective psychological features and background factors were statistically evaluated using stepwise multiple logistic regression analyses. In this study, we found that 'the self-evaluation of not having understood SLE at the time of starting SLE treatment' was the background factor significantly affecting depression or trait anxiety. 'No spouse' had a statistically significant effect on depression, and 'self-awareness as problems of side-effects due to steroids' had a statistically significant effect on state anxiety. We also found 'human relations among family members' and 'high daily steroid dosage' to be significantly correlated with suicide ideation. However, there were no correlations between the psychological features and 'disease activity at the time of investigation' or 'history of neuropsychiatric diseases'. In female SLE outpatients, performing psychological approaches focusing on 'understanding SLE at the beginning of treatment', 'the human relationships among family members', or 'issues related to steroid therapy' may be useful for the early treatment or prevention of various major mental problems.

Adult↗

PubMed2001

Cerebral atrophy related to corticotherapy in systemic lupus erythematosus (SLE).

The aim of this study was to evaluate the frequency and intensity of cerebral atrophy using CT scanning and the possible relation to corticosteroid therapy or disease in systemic lupus erythematosus (SLE) and to analyse the relationships between cerebral atrophy and activity disease and neuropsychiatric manifestations in lupus patients. We studied 107 consecutive SLE patients (American Rheumatology Association 1982 criteria) who were taking steroid drugs at the time and not selected for any particular manifestation (group 1). A complete clinical, neurological and laboratory evaluation was performed. The American College of Rheumatology's classification for neuropsychiatric manifestations and SLE disease activity index for activity were employed. Group 2 comprised 39 non-SLE patients with oral chronic steroid use (1 mg/k/day for more than 3 consecutive months); 50 normal individuals were the controls (group 3). There were no demographic differences between the groups. Brain CT was performed in all individuals and the frequency and the intensity (minimal, moderate and severe) of atrophy analysed, through well-defined measures and indices, by two neuroradiologists. Cerebral atrophy was significantly more frequent in groups 1 and 2 than in group 3, but with no significant difference between groups 1 and 2. The severity of cerebral atrophy was significantly higher in SLE patients (p<0.05), independent of steroid dose or duration of disease. In both groups no patient presented severe atrophy. Lupus patients with and without cerebral atrophy presented neuropsychiatric manifestations and activity disease in a similar proportion. The more frequent neuropsychiatric manifestation in lupus patients with cerebral atrophy was seizures (p<0.05). Chronic glucocorticoid therapy was responsible for cerebral atrophy, with a comparable incidence in both lupus and non-lupus patients compared to age and gender-matched normal subjects untreated with glucocorticoids. The disease activity was not related to cerebral atrophy in group 1 and seizures were the neurologic manifestation related to cerebral atrophy. The severity of the cerebral atrophy was independent of steroid dose, or duration of treatment. Moreover, the disease itself contributes to the severity of this process, but not to the development of cerebral atrophy.

Adrenal Cortex Hormones↗

PubMed1987

Failure of oral tolerance in (NZB X NZW)F1 mice is antigen specific and appears to parallel antibody patterns in human systemic lupus erythematosus (SLE).

Primary oral antigen exposure normally induces mucosal immunity and an active suppression of the systemic immune response. Patients with systemic lupus erythematosus (SLE) have increased antibodies to bovine gamma-globulin (BGG), which suggested a possible failure of oral tolerance in SLE. We examined this possibility in murine lupus. NZB/W females were fed BGG or saline and were subsequently immunized ip. Primary and secondary responses were assessed. At 1 month of age the mice tolerized normally in response to feeding with BGG but, at 4 months of age, not only did they not tolerize, the mice fed BGG had a 5- to 7-fold higher response to parenteral immunization than did the saline-fed mice. Control strain mice tolerized normally at both ages (a 5- to 10-fold lower response). Conversely, when fed ovalbumin, NZB/W females tolerized normally at both 1 and 4 months of age, and patients with SLE had normal levels of antibody to this antigen. However, we also found increased levels of antibodies to bovine casein in SLE patients, and found that NZB/W mice failed to orally tolerize with this antigen at either 1 or 4 months of age. Thus, the failure of oral tolerance in the NZB/W mice appears to be antigen specific and age dependent and, at least with respect to these three antigens, appears to parallel the antibody patterns seen in human SLE.

Administration, Oral↗

PubMed1995

Anti-DNA and anti-platelet specificities of SLE-derived autoantibodies: evidence for CDR2H mutations and CDR3H motifs.

Although polyreactivity appears to be a characteristic feature of natural autoantibodies, polyreactive anti-DNA autoantibodies can be derived both from patients with autoimmune disease and from normal individuals. It is unclear whether these autoantibodies differ depending on their origin, but previous studies from our laboratory have suggested that polyreactive systemic lupus erythematosus (SLE)-derived platelet-binding anti-DNA autoantibodies have more restricted antigen reactivity and greater functional activity than normal-derived polyreactive autoantibodies. The objective of the present study was to characterize the VH and VL region sequences of 10 human hybridoma anti-DNA autoantibodies derived from peripheral blood lymphocytes of different origins [SLE, rheumatoid arthritis (RA), or normal] to determine whether there are structural differences between these autoantibodies. We show that although some unmutated germline structures (VH and VL) are represented, these are not restricted to anti-DNA autoantibodies from normal individuals and that two normal-derived anti-DNA antibodies showed quite extensively mutated VH genes. However, these mutations, unlike those found in the CDR2H of several of the SLE-derived antibodies, did not appear to be antigen-selected. Three different amino acid motifs, putatively involved in antigen binding specificity, were observed in the CDR3H segments of some of the autoantibodies. One was the previously described YYGSG motif, which was found in a normal-derived anti-DNA autoantibody, while two new potential motifs were observed only in SLE-derived platelet-binding anti-DNA autoantibodies. These data suggest that antigenic and functional differences between SLE-derived and normal-derived platelet-binding anti-DNA autoantibodies may be due to antigen-selected mutations in the CDR2H and specific amino acid motifs in the CDR3H.

Amino Acid Sequence↗

PubMed1991

Binding profiles of anticardiolipin antibodies in sera from patients with SLE and infectious diseases.

Inhibition experiments were performed to study the specificity of IgG-class antibody, binding to cardiolipin immobilized onto a polystyrene surface, in sera from patients with systemic lupus erythematosus (SLE) or infection. Six different phospholipids (three anionic: cardiolipin, phosphatidylserine and phosphatidic acid, and three neutral: phosphatidylcholine, phosphatidylethanolamine and platelet activating factor), lipopolysaccharide from Salmonella Minnesota (ReLPS), strain Re595 and lipoteichoic acid from Streptococcus pyogenes were used as inhibitors, in the form of liposomes. Eight of fifteen SLE sera exhibited strong reactivity to phosphatidylserine liposomes; other anionic phospholipids, cardiolipin and phosphatidic acid, were less effective inhibitors. The binding was inhibited effectively only by cardiolipin in three of the SLE sera, and by none of the anionic phospholipids tested in the remaining four SLE sera. In most sera from patients with bacterial infections (including syphilis), anti-cardiolipin antibodies (ACA) were inhibited only by cardiolipin, but in some cases also by phosphatidic acid. In Gram-negative infections, ACA were inhibited by ReLPS more effectively than by cardiolipin. ReLPS also inhibited ACA in two of five chlamydial sera. Appreciable inhibition of ACA by phosphatidylserine did not occur in infections. Thus, in contrast to previous studies, broad reactivity to anionic phospholipids occurred in only about half of SLE sera. This pattern of polyreactivity was not seen in infections.

Antibody Specificity↗

PubMed2004

Prolactin as a modulator of B cell function: implications for SLE.

Prolactin is not only a lactigenic hormone but also an immunomodulator involved in lymphocyte survival, activation and proliferation. There is increasing data implicating prolactin in autoimmunity, and specifically in SLE. Increased serum prolactin levels have been reported in lupus patients of both genders, and have been associated with accelerated disease expression and early mortality in lupus-prone mice. Furthermore, suppression of prolactin secretion with bromocriptine provides beneficial effects in murine lupus, and perhaps in some SLE patients as well. Treatment with prolactin that causes mild to moderate hyperprolactinemia, similar to that present in SLE patients, breaks tolerance and induces a lupus-like illness in non-spontaneously autoimmune mice with a susceptible genetic background. These immuno stimulatory effects of prolactin are mediated by a decrease in negative selection and the maturation of autoreactive B cells to the follicular subset. Consistent with the fact that follicular B cells are T cell dependent, CD4+ T cells are necessary for the prolactin-mediated break down of B cell tolerance. In mice, the effects of prolactin on the immune system are genetically determined, suggesting that only a subset of SLE patients are likely to have a prolactin-responsive disease. The manipulation of serum prolactin or, even more specifically, follicular B cells that are susceptible to the immuno stimulatory effects of prolactin, may provide novel therapeutic options for those SLE patients with a prolactin-modulated disease.

Animals↗

PubMed2004

Autoantibodies in SLE but not in scleroderma react with protein-stripped nucleosomes.

Autoantibodies against nucleosomes (ANuA) are known to be sensitive markers for systemic lupus erythematosus (SLE), but their clinical relevance seemed to be limited because sera from patients with progressive systemic sclerosis (PSS) also showed positive reactions with conventional ANuA ELISA test systems (anti-Nu1 ELISA). It was generally assumed thatANuA were associated with both diseases. Using discontinuous sucrose gradient centrifugation to generate pure nucleosomes, we discovered by chance that at the 30-50% sucrose interface an antigen (Nu2) banded which was demonstrably free of non-histone components and histone H1. The two different nucleosome preparations, Nu1 and Nu2, were used in parallel as antigenic substrates in standardised ELISA tests to analyse sera from SLE (295 patients), PSS (119) and patients with other rheumatic diseases (101). With Nu1, 62% of the SLE and 52% of the PSS sera showed positive reactions. Two sera from patients suffering from Sjögren's syndrome (SS) and one from polymyositis were also positive. Using the Nu2 preparation, 58% of the SLE but none of the PSS sera showed a positive reaction. One serum from a patient with SS was also positive. It could be shown that it was the PSS-specific autoantigen Scl-70 in the nucleosome preparation (Nu1) which contributed to the positive reactions of the PSS sera in conventional ANuA test systems, whereas in the Nu2 preparation no remaining Scl-70 was detectable. The present study definitely proved that ANuA are highly and specifically associated with SLE but not with PSS.

Antibodies, Antinuclear↗

PubMed2005

Levels of complement in sera from inactive SLE patients, although decreased, do not influence in vitro uptake of apoptotic cells.

BACKGROUND: Accumulation of apoptotic cells is considered relevant in the pathogenesis of systemic lupus erythematosus (SLE). Complement factors facilitate the clearance of apoptotic cells and, when decreased, might result in an increased amount of apoptotic cells found in SLE patients. OBJECTIVE: To determine the influence of complement profiles from inactive SLE patients on the in vitro phagocytosis of apoptotic cells. METHODS: Consecutive SLE patients (n=98) with inactive disease (SLEDAI < or =4) and 20 healthy controls (HC) were included. Levels of CH50, C3, C4, C1q, and C1r were measured. Human peripheral blood monocytes were isolated from healthy controls and cultured for 7 days to obtain monocyte-derived macrophages (MDM). Jurkat cells were irradiated with UVB to induce apoptosis. Phagocytosis was tested by incubation of MDM with apoptotic cells in the presence of serum and quantified as phagocytosis index (number of Jurkat cells internalized by 100 macrophages). Serum from 20 patients with CH50<65%, 20 patients with CH50 > or =65%, and 20 HC were used in this assay. RESULTS: All HC and 37% of patients had normal complement levels. CH50 level was decreased in 21% of patients, C3 in 52%, C4 in 29%, C1q in 2% and C1r in 44% of patients. Between patients and HC, differences in level of CH50, C3 and C4 were statistically significant. No difference in phagocytosis index between HC and patients, irrespective of their CH50 level, was detected. No correlation was found between the respective complement levels and phagocytosis index. CONCLUSION: In most SLE patients with inactive disease, levels of one or more complement components are decreased. However, decreased levels of complement do not result in a significantly reduced in vitro uptake of apoptotic Jurkat cells by MDM.

Adult↗