Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Abnormal SLE mononuclear cell responses to PHA can be corrected by removal of adherent mononuclear cells. The present study demonstrates that cell-free supernatants from allogeneic adherent cell cultures inhibit lymphocyte response and that addition of indomethacin to cultures partly blocks the inhibitory effect of the resulting supernatant. Supernatants from SLE monocyte cultures suppressed allogeneic normal T cell responses by 36% (response in supernatant 33,515 +/- 3814 cpm, media control 51,947 +/- 3173 cpm) but normal monocyte culture supernatants did not suppress (48,384 +/- 4172 vs. 47,477 +/- 3221 cpm). Early (less than 24 hr) addition of indomethacin to monocyte cultures prevented elaboration of inhibitory material. In normals, indomethacin-treated supernatants were strikingly stimulatory (response 178% +/- 24 of control), whereas similarly treated supernatants of SLE monocyte cultures were not stimulatory (response 103% +/- 8 of control). The data indicate that a soluble inhibitor of lymphocyte blastogenesis is produced by SLE monocytes.
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PMID:Supressor monocytes in patients with systemic lupus erythematosus. Evidence of suppressor activity associated with a cell-free soluble product of monocytes. 644 33

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

Parameters of cell-mediated and humoral immunity were examined in 8 patients with clinically inactive SLE undergoing levamisole treatment. Lymphocyte transformation with PHA and PMW was temporarily increased in the first month of therapy; at the same time absolute numbers of peripheral blood lymphocytes, T cells and B cells increased slightly. However, these differences were not significant statistically. In 1 patient with a diminished percentage of T cells and an increased percentage of B cells, levamisole induced normalization. Antibodies to DNA decreased in 6 patients, while titres of ANA decreased only in one patient. Serum levels of C1q and C3 increased in 7 and 3 patients, respectively. Four patients were treated with levamisole for 12 months, during which time there was neither clinical exacerbation nor deterioration of renal function and the concomitant corticosteroid therapy could be reduced.
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PMID:Effect of levamisole on immunological parameters in patients with systemic lupus erythematosus. 696 71

The bone marrow granulocyte-macrophage progenitor cells (CFU-C) in patients with systemic lupus erythematosus (SLE) were estimated according to the double-layer soft agar system of Pike and Robinson. When nucleated narrow cells from patients with SLE were cultured with peripheral leukocytes from normal donors as a source on colony stimulating activity (CSA), colony counts (the term colony indicating aggregates of more than 50 cells) in active SLE were reduced significantly but cluster counts (cluster: 10 to 50 cells) were divided into two groups of markedly increased and decreased clusters. When normal nucleated marrow cells were cocultured in the overlayer with peripheral leukocytes of patients with SLE in he feeder layer, colony counts decrease significantly but cluster counts remained within the normal range. When CFU-C by normal nucleated marrow cells were studied in the presence of PHA- or LPS-induced CSA of peripheral leukocytes from patients with SLE, total colony and cluster counts decreased. These data indicate the granulomonocytopenia in SLE may result from the diminution of production of CSA in peripheral leukocytes and/or the direct impairment of growth and differentiation in progenitor cells of granulocytes and macrophages.
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PMID:Colony forming units in culture and colony stimulating activity of systemic lupus erythematosus. 697 21

We have succeeded in generating B cell colonies from freshly separated human peripheral blood by the double agar layer technique and expanding them in liquid culture for several weeks. Populations of cells enriched in B cells were placed into the upper layer with or without bacterial LPS. Although B cell colonies were observed without LPS, the addition of LPS to the cells in the upper agar layer increased the number of colonies. Also necessary for optimal B cell colony formation was the presence in the lower agar layer of either culture supernatant of PHA-stimulated mononuclear cells or purified T cells and PHA. Without such helper factors in the lower layer, only a few B cell colonies were observed in the upper layer. By using these techniques, peripheral blood lymphocytes from normal individuals and patients with active systemic lupus erythematosus (SLE) were studied for the generation of B cell colonies. Significantly more B cell colonies were observed in patients with SLE, using either kind of "helper" factor. In addition, T cells from normal individuals and patients were tested for their ability to help B cell colony formation. The SLE T cells were found to be defective in this function relative to normal T cells. Thus, although patients with SLE were hyperactive in forming B cell colonies, thier T cells were defective in supporting the formation of B cell colonies from normal individuals.
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PMID:Defective regulation of B lymphocyte colony formation in patients with systemic lupus erythematosus. 697 74

alpha 1 antitrypsin (alpha 1 AT) deficiency is a common genetic disorder seen in about 10% of the population. It predisposes to the development of a large number of inflammatory and immunologic disorders including rheumatoid arthritis, systemic lupus erythematosus, juvenile chronic arthritis, anterior uveitis, ankylosing spondylitis, fibrosing alveolitis and emphysema. We have investigated immunologic function in subjects with severe alpha 1 AT deficiency and demonstrated serum mediated enhancement of lymphocyte response to PHA and increased zymosan activation of mononuclear cells and neutrophils as measured by their chemiluminescence. These patients also have accelerated delayed hypersensitivity responses and increased levels of factor B, C3 and C5 but normal levels of immunoglobulin and other complement components. Such abnormalities in immunoregulation demonstrate a tendency to hyperreactivity that may contribute to disease predisposition.
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PMID:Immunoregulation by alpha 1 antitrypsin. 697 7

T cell colony growth in semisolid medium, a sensitive indicator of disease-associated lymphoycte defects, was found to be depressed in patients with PSS and RA. In both disorders, more pronounced abnormalities were observed after incubation with suboptimal concentrations of the polyclonal mitogen PHA. Depletion of monocytes by adherence to plastic surfaces of addition of the prostaglandin synthetase inhibitor indomethacin did not correct the growth abnormality observed in PSS. Reduced colony-forming activity could not be attributed to serum inhibitory factors. The cellular abnormalities detected in patients with these connective tissue diseases were less pronounced than those found in SLE patients.
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PMID:Reduced T lymphoid colony growth in patients with progressive systemic sclerosis and rheumatoid arthritis. 698 Feb 49

A comparative study of signal transduction through tyrosine phosphorylation process in peripheral blood lymphocytes from SLE patients and healthy subjects reveal some modifications in the phosphorylation pattern of SLE T lymphocytes. Thus, the level of constitutive tyrosine phosphorylation in resting SLE T lymphocytes is higher than in lymphocytes from healthy subjects. In SLE T lymphocytes, a cellular proteic substrate with an apparent molecular weight of about 37 kDa is constitutively phosphorylated. Some differences in the pattern of phosphorylation are obvious in lectin (Con A, PHA)-activated T lymphocytes. Thus, Con A activation enhances the phosphorylation of cellular substrates with molecular weight in the range of 55-80 kDa from SLE T lymphocytes. Moreover, the 21 kDa substrate is also hyperphosphorylated after PHA activation of SLE lymphocytes.
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PMID:Signal transduction in T lymphocytes of SLE patients: lectin-activated phosphorylation on tyrosine. 753 65

In autoimmune diseases striking abnormalities of T and B cell activation and of cytokine production are present. In 14 patients with autoimmune hemolytic anemia (AIHA), idiopathic or in the course of: lymphoma, B hepatitis, carcinoma, drug therapy (alpha-methyldopa), systemic lupus erythematosus (SLE), and not yet submitted to immunosuppressive therapy, the PBL proliferative response to PHA and the IL1 alpha, IL2, IL4 and IL2R serum levels have been valued. While the stimulation index of PBL was strongly reduced in 10 cases (64 +/- 56 vs 138 +/- 45 in the control group), IL1 alpha, IL2 and IL2R were greatly increased in all the patients, and IL4 in 5 (IL1 alpha :199 +/- 268 pg/ml in patients vs 0.30 +/- 0.2 in controls; IL2:716 +/- 311 pg/ml vs 16 +/- 4; IL4:29 +/- 13 pg/ml vs 13 +/- 7; IL2R:1233 +/- 471 U/ml vs 256 +/- 114). Cytokine serum levels were not related with the associated disease, with the CD4+ and CD8+ cells absolute number or with PBL blastogenic in vitro response. The high serum levels of cytokines and IL2R suggest that in AIHA there exist a CD4+ lymphocyte hyperactivation (the low proliferative response of PBL might imply a temporary functional exhaustion of T lymphocytes) as in the other autoimmune diseases.
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PMID:High cytokine serum levels in patients with autoimmune hemolytic anemia (AIHA). 785 62

PBMC proliferation in patients with SLE was assessed by incorporation of 3H-Tdr in an accessory cell-dependent response to anti-CD2 specific monoclonal antibody. The response was compared to monoclonal anti-CD3 and PHA response. There was a marked decrease in the response to anti-CD2 in SLE patients (9257 +/- 8543) than in normal controls (20619 +/- 15279) (P < 0.005). It was more obvious in 8 patients with less active and untreated disease, but not in 10 patients with less active or inactive disease. In contrast, no statistical difference was noted in the response to anti-CD3 and PHA between SLE patients and normal controls. We also examined the response of purified T cells to anti-CD2 and the response was depressed in SLE, but no marked decrease in the response to anti-CD3 was found in SLE patients. Our results demonstrate that SLE patients with active disease have T cells that respond poorly to CD2 activation, but that response via the CD3/TCR complex is essentially intact. It might be reflect intrinsic T cell defects in some SLE patients.
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PMID:[CD2-mediated T-lymphocyte proliferation in patients with systemic lupus erythematosus]. 790 69


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