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)

The response of peripheral blood lymphocytes to the phytomitogens, PHA, Con A, and PWM, was evaluated in 30 SLE patients and in 30 age, sex, and race-matched controls using dose and time responses. The proliferative response to the three phytomitogens was not depressed in this group of subacute and chronic SLE patients. Active lupus nephritis and a slow acetylator phenotype were associated with a decreased lymphocyte response. The incidence of a slow acetylator phenotype in spontaneous SLE was 68%. In interpreting the lymphocyte response to phytomitogens, the importance of a clear definition of the SLE group under study, the activity of the disease, and treatment status are emphasized.
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PMID:Peripheral blood lymphocyte response to phytomitogens in systemic lupus erythematosus. 123 8

In our previous report, we demonstrated that the functions of phagocytes and lymphocytes were defective in patients with systemic lupus erythematosus (SLE). In an attempt to further clarify the defective mechanisms of these cells, 25 active SLE, 10 bronchial asthma patients (BA) on corticosteroids and 25 age and sex-matched normal individuals were investigated for the expression of membraneous C3b receptors, ionophore-induced 45Ca(2+)-uptake, mitochondrial potentials and phagocytic activity of neutrophils. We found decreased expression of C3b receptors on SLE PMN in both resting (37.2 +/- 3.7% of the normal controls) and FMLP-stimulated (68.3 +/- 7.1% of the normal controls) conditions, whereas the C3b receptor expression on BA-PMN receiving long-term steroid treatment was not different from normal controls. This suggests that the defective phagocytosis of SLE PMN is in the recognition, but not in the ingestion phase because of the normal function of Ca(2+)-influx and mitochondrial activity in SLE PMN. On the other hand, hyporesponsiveness to PHA stimulation (stimulation index: 127.4 +/- 46.3 in SLE vs. 311.2 +/- 30.4 in normals, p = 0.0077) was a distinct cell-mediated immune abnormality in our SLE patients. We measured the membrane potential of individual cells using 3,3'-dihexyloxacarbocyanin and found hyperpolarization in resting SLE lymphocytes. However, the membrane polarization of SLE lymphocytes became lower than that of normal cells after PHA stimulation for 3 days. A similar tendency was also found in Na(+)-K(+)-dependent ATPase activity in SLE lymphocytes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Defective expression of neutrophil C3b receptors and impaired lymphocyte Na(+)-K(+)-ATPase activity in patients with systemic lupus erythematosus. 166 18

A previous study demonstrated that interferon was present in the serum of 30% of the patients with systemic lupus erythematosus (SLE), which was significantly higher than the 4.5% found in normal controls. We also recently reported that interferon production was deficient from SLE mononuclear cells, which has been attributed to immunodeficiency of the lymphocytes. In this study, interferon measurement included lymphocytes obtained from peripheral blood (PB), synovial fluid (SF) and synovial tissue (ST) in patients with rheumatoid arthritis (RA) and ankylosing spondylitis (AS). PB from normal subjects (NS) was used as a control. The results showed with PHA stimulation, that the interferon level in PBL (L = lymphocyte) in NS (70.0 +/- 67.5) was significantly higher when compared with PBL in RA (27.9 +/- 21.6). However, there was no difference between PBL in NS and AS. With ConA stimulation, the interferon level was significantly higher in the PBL of NS (130 +/- 59) and as compared with the PBL in RA (83.6 +/- 53.5). The SFL in RA (67.8 +/- 31.1) and the STL in RA (77.2 +/- 93.2) were also significantly different. It is concluded that interferon production was deficient not only in PBL in RA, but also in SF and STL in RA. The reduced interferon production from PB, SF and ST lymphocytes in RA patients may be due to previous release or immunodeficiency. Lymphocyte interferon production was normal in AS, which suggests that the lymphocyte abnormality between RA and AS may be different.
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PMID:Interferon production from peripheral blood, synovial fluid, and synovial tissue lymphocytes in patients with rheumatoid arthritis and ankylosing spondylitis. 170 7

The role of interleukin-4 (IL-4) and interferon-gamma (IFN-gamma) in the pathogenesis of the collagen vascular diseases was studied. The serum level of IL-4 was decreased in patients with systemic lupus erythematosus (SLE) and mixed connective tissue disease (MCTD), and was variable in patients with rheumatoid arthritis (RA). The serum level of IFN-gamma was increased in patients with SLE, MCTD and RA. In patients with SLE, there was an inverse correlation between the levels of IL-4 and IFN-gamma. The proliferation and immunoglobulin production of the high-density-B cells in response to IL-4 was suppressed in normal controls, although the degree of suppression was less in patients with SLE. Cell cycle analysis using ethidium bromide demonstrated the similar findings. These data suggest that IL-4 and IFN-gamma might participate in regulating both of growth and differentiation of B cells in vivo. However, immunoglobulin production by whole B cells in response to IL-2 or PHA-induced T-cell factor was extensively facilitated by IFN-gamma in patients with SLE. It is possible that IFN-gamma enhances the differentiation of already-activated B cells, and that polyclonal B cell activation is promoted. Therefore, the failure of the regulatory mechanism by these cytokines might be related to the pathogenesis of these diseases.
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PMID:[Relationship between serum interleukin-4 or interferon-gamma level and B cell abnormality in patients with collagen vascular diseases]. 176 43

Using various monoclonal antibodies to T cell activation molecules it has been shown that purified T cells from patients with active systemic lupus erythematosus overexpress the 4F2, IL-2R (CD25), HLA-DR and T10 antigens. T cells from patients with inactive disease had increased expression of VLA-1 and HLA-DR. Increased T10 expression on T cells from patients with active disease correlated inversely with the production of IL-2, whereas expression of CD25 was slightly increased after 3-day culture with either PHA or anti-CD3. These results provide further evidence of the in vivo activation of T cells in SLE and suggest that such activation comes slowly to a halt upon disease remission.
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PMID:Activation markers on peripheral blood T cells from patients with active or inactive systemic lupus erythematosus. Correlation with proliferative responses and production of IL-2. 181 97

The leukotriene B4 (LTB4) releasing capacities of monocytes and polymorphonuclear leukocytes (PMN) were studied using a specific radioimmunoassay in 28 patients with systemic lupus erythematosus (SLE) and 9 normal controls. LTB4 release from both monocytes (7.3 +/- 3.3 ng) and PMN (6.6 +/- 3.4 ng) in SLE patients was decreased compared with that (15.2 +/- 4.3 ng for monocytes, 20.7 +/- 4.5 ng for PMN) in normal controls. There were no differences in the releasing capacities of monocytes and PMN between patients with active and inactive disease. LTB4 suppressed lymphocyte blastogenesis by PHA-P and induced suppressor cells. The significance of the decreased release of LTB4 from monocytes and PMN in SLE patients was discussed.
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PMID:Decreased release of leukotriene B4 from monocytes and polymorphonuclear leukocytes in patients with systemic lupus erythematosus. 185 11

Antibody to double-stranded DNA is a specific marker for systemic lupus erythematosus. The recommended method for detection of this antibody is immunofluorescence. Haemagglutination was developed and the results of antibody detection were evaluated with those obtained by immunofluorescence. Human group O erythrocytes were treated with glutaraldehyde and coated with DNA from calf thymus. Testing in 169 active and inactive SLE sera, 59 sera were positive and 91 sera were negative by both methods. Five sera were negative by haemagglutination but positive by immunofluorescence. Fourteen sera with low haemagglutination titer were negative by immunofluorescence. The correlation between the results obtained by both methods were highly significance with contingency coefficient of 0.61 and correlation coefficient between the results of 78 sera positive by both or either method was 0.74 (p less than 0.001). Sixty-three sera from blood donors and seventy sera from pregnant women were negative by the two techniques. PHA is simpler, quicker and can be assayed in laboratories without the use of fluorescent microscope. It can be established as a very useful alternative test to immunofluorescence.
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PMID:A comparison of passive haemagglutination test and immunofluorescent test for antibody to native deoxyribonucleic acid. 186 Nov 30

To determine whether there is an intrinsic defect in T cells from patients with systemic lupus erythematosus (SLE), we studied signal transduction systems, assaying the total protein kinase C (PKC) levels and the phorbol myristate acetate (PMA)-induced activation of PKC in PHA-treated T cells. T cells from SLE patients showed a decrease in proliferation in response to PMA, but not to PHA, thereby suggesting the existence of an intrinsic abnormality in the PKC-mediated activation pathway. Total PKC activity in the T cells from SLE patients was significantly decreased. Although stimulation with PMA induced a translocation of PKC from the cytosol to the particulate fraction, translocated PKC activity after 2 nM PMA treatment was decreased in the SLE T cells. Furthermore, PMA-induced phosphorylation of 80-kDa substrates was also decreased in SLE T cells. These results suggest that there is a reduced PKC activity and an impaired PKC activation in response to PMA in the SLE T cells, a finding which may explain, if partially, the defect in T cell activation in patients with SLE.
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PMID:A defect in the protein kinase C system in T cells from patients with systemic lupus erythematosus. 207 May 68

HLA-DP+ T cells in peripheral blood from 23 patients with systemic lupus erythematosus (SLE) were examined using two-colour flow cytometry analysis. A marked increase of HLA-DP+ T cells was observed in patients with SLE (20.5-98.7%; 59.8 +/- 20.8%) in comparison to normal subjects (1.3-20.6%; 11.1 +/- 7.2%), and the ratio of these cells greatly exceeded that of the HLA-DR+ T cells (6.5-49.1%; 21.5 +/- 12.7%). This high frequency of HLA-DP+ T cells in patients with active SLE decreased with prednisolone therapy. When the lymphocytes from normal subjects were stimulated with PHA in vitro, HLA-DP+ T cells increased from 1.8 to 59.2%. Therefore, it appears that the HLA-DP antigen expression on T cells is a practical marker for monitoring changes in the proportion of activated T cells in patients with SLE during the course of therapy.
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PMID:HLA-DP-positive T cells in patients with systemic lupus erythematosus. 212 50

TNF-alpha is a macrophage-derived cytokine with diverse biologic activities, including potent immunomodulatory effects. In vitro studies have implied that TNF-alpha has predominantly proinflammatory and immunostimulatory effects, but paradoxically in vivo studies have demonstrated that administration of TNF-alpha suppresses murine lupus. To assess the effects of TNF-alpha on immune function in normal mice, we treated C57BL/6 mice with recombinant murine TNF-alpha (10 micrograms i.p.) or PBS on alternate days for up to 8 wk. Administration of TNF-alpha decreased the percentage of splenic T and B cells and increased the percentage of splenic macrophages without significantly altering the total number of mononuclear cells. Administration of TNF-alpha also caused progressive inhibition of splenic lymphocyte function, out of proportion to the quantitative reduction in B and T cells. After 8 wk of therapy, the proliferative responses of splenic lymphocytes to Con A, PHA, and LPS were reduced by 100, 90, and 60%, respectively, in treated mice compared with control mice. The reduction in T cell proliferation was due primarily to alteration of accessory cell function rather than direct inhibition of T cell function. Treatment with TNF-alpha markedly inhibited T cell cytotoxicity induced by immunization with allogenic target cells, and it virtually ablated NK cell activity. Inhibition of these in vitro tests of lymphocyte function correlated with inhibition of delayed type hypersensitivity in vivo. In contrast, treatment with TNF-alpha did not impair humoral immunity. These findings imply that TNF-alpha may affect cell-mediated immunity more profoundly than humoral immunity. This observation may be relevant to the mechanism whereby TNF-alpha suppresses murine lupus.
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PMID:Effects of recombinant murine tumor necrosis factor-alpha on immune function. 230 39


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