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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The immunological responsiveness of a panel of 17 patients with systemic lupus erythematosus (SLE) was studied in an in vitro model of xenogeneic sensitization against mouse lymphoid cells. Generation of cytotoxic thymus-derived (T) cells evaluated by a chromium release assay against labeled target cells was found to be drastically impaired in these lupus patients. Such depression was independent of drug therapy at the time of the study, clinical status, and other immunological parameters such as antibodies against native DNA, complement levels, cryoglobulinemia, circulating immune complexes, or T- and bone marrow-derived (B)-cell numbers. In contrast to the cytotoxic response, the proliferative responses to phytohemagglutinin, to allogeneic lymphocytes, and to xenogeneic lymphocytes were not significantly different from those of normal individuals. The latter response was shown to be H-2 restricted with the primed lymphocyte test. These results suggest the presence of a selective defect in the generation or in the expression of killer cells rather than a deficiency in antigen recognition by T cells. The role of serum factor(s) was examined by educating the lymphocytes of normal subjects in the presence of serum from SLE patients. Such manipulation affected both the generation of killer cells and the proliferative response. Finally our observations indicate that depression of cell-mediated immunity in SLE patients may be associated with several mechanisms including a cellular one, specifically affecting the generation of killer T cells, and a humoral one possibly as a result of antilymphocytic antibodies and(or) immune complexes.
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PMID:Selective depression of the xenogeneic cell-mediated lympholysis in systemic lupus erythematosus. 11 Aug 33

Passive hemagglutination (PHA) and hemolysis (PHL) tests using chromium chloride-treated sheep red blood cells were developed to detect and measure the anti-DNA antibodies. Sonication of native DNA was found to prevent the incidence of non-specific agglutination. Sheep red cells were coated with double-stranded DNA (dsDNA) which had been sonicated and treated with nuclease S1 to digest the single-stranded regions in the DNA. The specificities for dsDNA-coated cells were checked by inhibition studies in PHA test and plaque assay. In clinical studies fairly close correlations were found between the antibodies to DNA and the activity of the disease in patients with systemic lupus erythematosus (SLE). Complement-fixing antibodies were detected in most of SLE patients with active lupus nephritis, but rarely in those in remission. Anticomplementary activity seemed to be negligible in PHL test. These tests are simple and may be useful to the diagnosis and the management of SLE.
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PMID:Passive hemagglutination and hemolysis tests for the detection of anti-DNA antibody. 35 55

Criteria for the recognition of systemic lupus erythematosus (SLE) were applied to 362 subjects exposed to trichloroethylene, trichloroethane, inorganic chromium, and other chemicals in water obtained from wells in an industrially contaminated aquifer in Tucson, Arizona. Their antinuclear autoantibodies were measured by fluorescence (FANA) in serum. Ten patients with clinical SLE and/or other collagen-vascular diseases were considered separately. Results were compared to an Arizona control group, to published series, and to laboratory controls. Frequencies of each of 10 ARA symptoms were higher in exposed subjects than in any comparison group except those with clinical SLE. The number of subjects than in any comparison group except those with clinical SLE. The number of subjects with 4 or more symptoms was 2.3 times higher compared to referent women and men. FANA titers greater than 1:80 was approximately 2.3 times higher in women but equally frequent in men as in laboratory controls. ARA score and FANA rank were correlated with a coefficient (cc) of .1251, r2 = .0205 (p less than 0.036) in women and this correlation was almost statistically significant in men cc = .1282, r2 = .0253 (p less than 0.059). In control men and women neither correlation was significant. Long-term low-dose exposure to TCE and other chemicals in contaminated well water significantly increased symptoms of lupus erythematosus as perceived by the ARA score and the increased FANA titers.
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PMID:Prevalence of symptoms of systemic lupus erythematosus (SLE) and of fluorescent antinuclear antibodies associated with chronic exposure to trichloroethylene and other chemicals in well water. 174 91

The binding and functional activities of platelet-binding hybridoma autoantibodies from SLE patients were compared with those derived from normal individuals. Twenty-nine SLE-derived hybridoma antibodies and 20 normal-derived hybridoma antibodies were analyzed for binding to glutaraldehyde fixed platelets, dDNA and phospholipids, and for lupus anticoagulant activity. Twenty-four of the 29 SLE-derived antibodies and 9 of the 20 normal-derived antibodies showed one or more activities in these assays. Of the 24 SLE-derived antibodies, 8 (33.3%) were reactive in only one assay (monospecific), while the other 16 (66.7%) had more than one of these activities (polyspecific). In contrast, none (0%) of the 9 normal-derived antibodies with known activities were monospecific, while all 9 (100%) showed polyspecificity. Statistical analyses demonstrated that there was no correlation of anti-DNA activity with anti-platelet and most anti-phospholipid activities for the SLE-derived antibodies, and strong positive correlations between these reactivities for the normal-derived antibodies. Similarly, differences were observed in Western blotting analyses; SLE-derived antibodies bound more specifically to individual platelet proteins than normal-derived antibodies. Moreover, in chromium-51 release assays, all of the SLE-derived platelet-binding antibodies were cytotoxic to platelets, while none of the normal-derived platelet-binding antibodies showed significant cytotoxicity. Our results suggest that hybridoma platelet-binding autoantibodies derived from SLE patients exhibit greater antigen specificity and functional activity than similar antibodies derived from normal individuals.
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PMID:Differences between human hybridoma platelet-binding antibodies derived from systemic lupus erythematosus patients and normal individuals. 212 49

The patterns of migration of lymphoid cells from autoimmune-prone MRL-lpr/lpr, C57BL/6-lpr/lpr, MRL-+/+, and NZB mice were compared to those from sex and age-matched, normal CBA, C57BL/6, and BALB/C mice. Chromium-51-labelled spleen and lymph node cells from all autoimmune mice tested homed preferentially to the spleen relative to lymph node of the recipient strain. The data indicate that defects in lymphocyte trafficking are widespread in murine lupus and suggest a role for abnormal lymphocyte migration in the pathogenesis of this disease.
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PMID:Aberrant lymphocyte trafficking in murine systemic lupus erythematosus. 379 57

Using as target cells chicken erythrocytes labelled with chromium 51Cr the cytotoxic activity (spontaneous and induced with PHA and Con A mitogens) of peripheral blood lymphocytes was studied in patients with multiple sclerosis. The control group comprised healthy subjects, patients with systemic lupus erythematosus and other central nervous system diseases. No changes were observed in the cytotoxic activity of lymphocytes of patients with multiple sclerosis without respect to the course and a duration of the disease process. On the other hand, in patients with SLE a decrease of cytotoxic activity was observed in vitro, both spontaneous activity (p less than 0.01) and mitogen-induced (p less than 0.05) as compared with other group of patients.
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PMID:[In vitro cytotoxic activity of peripheral blood lymphocytes in patients with multiple sclerosis. Preliminary report]. 666 8

Plasma protein loss via gastrointestinal tract was determined in 24 patients with clinical and laboratory data for manifested nephrosis syndrome, 21 of them being with various histological forms of chronic glomerulonephritis, 2--with disseminated lupus erythematosus and 1--with renal amyloidosis. Isotope labelled chromium trichloride was intravenously applied, marking the albumin pool in a dose of 0.5 micro curie (20 KBq/kg body weight). In four patients an increased fecal radio-activity was established amounting to 1.00 to 2.63 per cent of the injected dose for 96 hours. The possible causes for that phenomenon are discussed as well as its significance in the advancement of nephrosis syndrome.
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PMID:[Plasma protein loss via the gastrointestinal tract in nephrotic syndrome patients]. 667 79

Spontaneous cytotoxicity mediated by natural killer (NK) cells is impaired in several human diseases including systemic lupus erythematosus (SLE). The present study was designed to describe factors in SLE sera which suppress the NK function of unfractionated mononuclear cells and NK enriched suspensions. NK activity was determined in 19 SLE patients and 25 normal controls by a standard chromium release assay. Sera obtained from SLE patients suppressed normal NK activity by an average of 29.4%. The presence of anti-lymphocyte antibodies (ALA) of the IgM class which were reactive with unfractionated mononuclear cells or the NK cell enriched OKM1 positive subset correlated with serum-mediated suppression. NK inhibitory SLE sera did not interfere with normal effector-target conjugate formation. These results demonstrate the modulatory effects of immune aggregates and ALA on lymphocyte function in SLE. These factors suppress NK function without evidence of lymphocyte cell death or inhibition of NK effector cell binding to tumour targets.
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PMID:Natural cytotoxicity in systemic lupus erythematosus: mechanisms of suppression by inhibitory serum factors. 688 8

The natural killer (NK) cell activity in fifteen systemic lupus erythematosus (SLE) patients was investigated by employing 51-chromium- (51Cr) release microcytotoxicity and single cell cytotoxicity assays against K562 target cells. Although the SLE patients as a group had depressed NK function in the 51Cr-release assay compared to normal subjects (p less than 0.005), those with clinically active disease displayed the greatest impairment in this activity (p less than 0.001). Active SLE patients were deficient in overall NK activity (Vmax) (p less than 0.005) but had normal percentages of potentially cytotoxic target binding cells (TBC). These TBC, however, were unable to normally kill bound target cells (p less than 0.01), which is indicative of a deficiency of "active" NK cells (p less than 0.005). Those NK cells with intact cytotoxic capabilities could "recycle" and repeat the lytic sequence normally. Exposure of normal lymphocytes to SLE sera did not impair any phase of NK function. These studies indicate that defective NK activity in SLE is secondary to an abnormality in the lytic event itself and is not due to a deficiency of NK cells, an abnormality in target binding, or an inability of NK cells to lyse multiple targets. Additionally, serum factors do not appear to play a major etiologic role in the cytotoxic abnormalities of these patients.
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PMID:Abnormal natural killer cell activity in systemic lupus erythematosus: an intrinsic defect in the lytic event. 711 39

The presenting clinical pictures and courses of seven patients with thrombocytopenia, decreased megakaryocytes in the marrow, and minimal changes in other hematopoietic cell lines are described. Little information exists in the literature on such patients. Initial bone marrow aspiration and biopsy in all patients showed decreased megakaryocytes with an otherwise normal marrow. Erythrocyte mean corpuscular volume was elevated in five of seven patients. Bone marrow karyotypes of six of the seven patients were normal. Chromium-51 platelet survival studies with platelet sizing, done in five of the seven patients, showed normal results. In two patients the course progressed to aplastic anemia. One of these died 9 months after presentation, and one responded dramatically to lithium. One patient developed preleukemia and died. The other four patients have remained thrombocytopenic but clinically stable. No useful therapy was identified. The differential diagnosis of such patients should include idiopathic thrombocytopenic purpura with misinterpretation of morphologic findings, hereditary and acquired aplastic anemia, preleukemia, and systemic lupus erythematosus.
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PMID:Thrombocytopenia with decreased megakaryocytes. Evaluation and prognosis. 719 25


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