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

In vitro irradiation with long wavelength ultraviolet light (UV-A), in clinically relevant dosages, of a natural killer cell line containing cell preparations from 17 control subjects reduced natural killer cell cytotoxicity with the cell line K562 as target. The spontaneous function of natural killer cells from 12 patients with systemic lupus erythematosus (SLE) correlated inversely with the one hour erythrocyte sedimentation rate, but not with glucocorticoid doses. After UV-A exposure, natural killer cells from patients with SLE exert either increased or decreased cytotoxicity, and the direction of change is inversely correlated with the spontaneous natural killer cell function.
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PMID:Effects of ultraviolet irradiation on natural killer cell function in systemic lupus erythematosus. 161 54

Systemic lupus erythematosus (SLE) patients at advanced stages of the disease have an interferon inhibitor in the blood circulation. This inhibitor can block antiviral activity of all three types of human interferons and can significantly reduce the synthesis of interferon alpha by the treated lymphocytes obtained from normal healthy individuals. Available evidence suggests that inhibitor activity is neither because of the antibody to interferon nor due to high level of protease-like activity in the plasma. The inhibitor has also been shown to be effective in eliminating the interferon-mediated enhancement of natural killer cell activity. Interferon inhibitory activity was not detected in any of the sera taken from normal healthy individuals. Identification and characterization of interferon inhibitor has direct bearing upon effective utilization of interferons in the clinic.
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PMID:Interferon inhibitor in the blood of patients with systemic lupus erythematosus. 171 34

The influence of dietary fat on autoimmunity in lupus-prone (NZB x NZW)F1 mice has been demonstrated. In defining further the effects of dietary lipid on the immune system of this strain, female weanling mice were placed on four diets differing in quantity and type of fat. Their immunologic response was then studied by a variety of tests at 4 and 7 mo of age. Few differences were seen among the four groups at 4 mo of age. At 7 mo of age, however, the mice receiving diets high in saturated and unsaturated fats had a reduced mitogenic response to T cell mitogens and an enhanced response to the B cell mitogen LPS. Immunoglobulin levels and delayed hypersensitivity responses did not show any consistent differences among the diet groups. At 7 mo, however, mice receiving diets high in unsaturated fat demonstrated hyperresponsiveness to injected sheep red blood cells as measured by the hemolytic plaque technique. In addition, peritoneal leukocytes from the same diet group exhibited an increased response to bromelain-treated autologous erythrocytes which was decreased after treatment with anti-Thy-1 antiserum and complement. Phagocytosis by peritoneal macrophages was significantly decreased in the animals fed high-fat diets, particular high saturated fat. Similarly, natural killer cell activity was markedly reduced in the mice with a high intake of saturated lipid, a finding which correlated with the in vitro production of interferon. These results indicate that diets high in fat influence immune responses and thus can affect the onset and severity of autoimmune disease. A low-fat diet can reduce the development of disease by maintaining normal immune responses. The data also suggest that unsaturated fat may influence T helper cell activity and therefore antibody production, whereas saturated fats may affect cellular immune responses which are dependent on membrane contact.
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PMID:Dietary fat and immune function. I. Antibody responses, lymphocyte and accessory cell function in (NZB x NZW)F1 mice. 241 89

We studied the effects of recombinant murine tumor necrosis factor-alpha (TNF-alpha) on autoimmune disease in lupus-prone NZB/NZW F1 (B/W) mice. Treatment with TNF-alpha, begun after the onset of clinical disease, improved survival relative to control mice: at age 10 months, 92% of mice treated with TNF-alpha were alive compared with 42% of control mice (P less than 0.05). Administration of TNF-alpha delayed the progression of renal disease, but sustained therapy did not prevent the eventual development of severe nephritis. Despite the improvement in survival, treatment with TNF-alpha did not inhibit anti-dsDNA antibody production. However, it accelerated T lymphocytopenia and abolished natural killer cell activity. These observations suggest that TNF-alpha may retard murine lupus in B/W mice through effects on cellular rather than humoral mechanisms. Our findings also indicate that the beneficial effects of TNF-alpha cannot be sustained indefinitely by chronic therapy.
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PMID:Chronic therapy with recombinant tumor necrosis factor-alpha in autoimmune NZB/NZW F1 mice. 275 98

Systemic lupus erythematosus (SLE) is characterized by a variety of profound T-cell abnormalities among which are decreased cytotoxic capacity measured by allogeneic cell-mediated lympholysis (CML), natural killer cell (NK) activity, and decreased lymphokine production. In a group of 13 patients with active SLE, allogeneic CML, tested by a 4-hr 51Cr-release assay, was 18.2 +/- 2.7% while in the group of normal individuals CML was 41.2 +/- 2.7%. If optimal doses of affinity-purified interleukin-2 (IL-2) were present during the mixed lymphocyte culture, the CML of SLE patients was increased to normal levels (40.4 +/- 4.0%). In contrast, interferon-alpha (IFN-alpha) increased (but not significantly) the levels of CML. Mixed lymphocyte reaction, tested by tritiated thymidine incorporation, was also decreased in the group of patients (14,820 +/- 815 cpm vs 28,972 +/- 5880 cpm in normals) and it was increased to normal levels if IL-2, but not IFN-alpha was added to the cultures. NK activity was decreased in the group of patients tested by 51Cr-release assay, harvested at 6 and 18 hr. IL-2 increased the NK activity up to normal levels, while IFN-alpha was only partially efficacious. These results demonstrate that IL-2, but not IFN-alpha, can potentiate or even fully restore the deficient cytotoxic effector function of peripheral mononuclear cells in patients with SLE.
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PMID:Interleukin-2 restores the depressed allogeneic cell-mediated lympholysis and natural killer cell activity in patients with systemic lupus erythematosus. 315 17

Interleukin-2 (IL-2) production in vitro is depressed in systemic lupus erythematosus (SLE) patients. It is not known whether this abnormality is caused by a defect in the producer lymphocytes or by excessive suppression. We report that removal of OKT8 (Leu 2a)+ cells increased the IL-2 production by in vitro-stimulated lymphocytes to normal or above normal levels in 19 of 21 SLE patients. This increase was more apparent in those patients with clinically inactive disease and/or receiving less than 7.5 mg of prednisone. Removal of OKT8+ cells from normals did not significantly increase IL-2 activity. SLE, but not normal, OKT8+ cells decreased IL-2 production when added back to autologous OKT8-depleted cells. In some experiments, OKT8+ cells from normal donors also suppressed IL-2 production in SLE. This result suggests that the defect in IL-2 production is complex and may involve multiple cell interactions. Three lines of evidence suggest that the SLE OKT8+ cells actively inhibit the production of IL-2 rather than passively absorb this lymphokine: (a) only 3.2% of SLE lymphocytes expressed IL-2 receptors as detected with anti-Tac; (b) freshly prepared SLE lymphocytes did not absorb IL-2; and (c) cell-free supernatants from SLE OKT8+ cells inhibited IL-2 production, but not IL-2 activity. Double-labeling studies by flow cytometry revealed that 19.3% of SLE OKT8+ cells were also Ia-positive, and approximately 33% co-expressed the natural killer cell marker, HNK-1 (Leu 7). Removal of Leu 7+ cells also significantly elevated IL-2 production in SLE. These studies suggest that one or more circulating mononuclear cell subsets in SLE patients can suppress IL-2 production and that one subset may possibly belong to a non-T, non-B "third mononuclear population."
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PMID:Correction of interleukin-2 production in patients with systemic lupus erythematosus by removal of spontaneously activated suppressor cells. 315 52

Treatment of patients suffering from systemic lupus erythematosus with vitamin A (100,000 U daily for 2 weeks) resulted in an enhancement of antibody-dependent cell-mediated cytotoxicity, natural killer cell activity and blastogenic response to plant mitogens and interleukin-2 (IL-2).
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PMID:Effect of vitamin A treatment on the immune reactivity of patients with systemic lupus erythematosus. 318 59

Selenium is a trace mineral and a required nutrient for animals and humans. Selenium intake appears to be inversely correlated with the risk of developing cancer. Since immunological effects of selenium have been described we studied the capacity of selenium to modify the lupus-like disease of NZB/NZW female mice. Our data indicate that selenium supplementation (sodium selenite 4 parts per million in the drinking water) significantly improves survival in these autoimmune mice: mean survival 55.6 +/- 4.6 weeks (mean +/- s.e.) for treated mice versus 36.1 +/- 1.9 weeks for controls (P less than 0.04). Additionally, selenium supplemented mice had significantly higher natural killer cell activity (P less than 0.001). However, no obvious effects of selenium supplementation on autoantibody production were observed.
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PMID:Improved survival in murine lupus as the result of selenium supplementation. 326 35

We studied natural killer cell-mediated (NKCM) activity and its enhancement by interleukin-2 (IL-2) in 15 patients with mixed connective tissue disease (MCTD). The mean baseline NKCM activity of peripheral blood mononuclear cells (MNC) against K562 target cells in the 51Cr release assay was found to be similar to that found in age/sex-matched controls. MCTD patients' cells, however, responded significatively less to IL-2 induction of NKCM than did those of the controls. Using the single-cell agarose NK assay, we found that MCTD patients have a small number of active NK cells that exhibit a high rate of recycling capacity in the baseline state. These preactivated cells could not be stimulated further by IL-2. In two MCTD patients the response to IL-2 was nil, and in the serum from both of them we found an IgM inhibitory factor of such IL-2 induced enhancement. This factor could be absorbed only partially by normal MNC and NK cell-depleted MNC but completely by an IL-2-dependent T-cell line, suggesting that the inhibitory factor may be acting on the IL-2 receptor. These findings seem to be different from those reported in systemic lupus erythematosus and strengthen the notion that MCTD is due to a different immunoregulatory aberration.
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PMID:Natural killer cell-mediated activity in mixed connective tissue disease and its response to induction by interleukin-2. 661 47

With strictly selected controls natural killer cell activity was evaluated in 10 untreated patients with systemic lupus erythematosus. Natural killer levels of the patients were significantly lower than those of the age- and sex-matched normal controls. Natural killer levels, however, did not correlate with disease activity.
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PMID:Natural killer cell activity in untreated systemic lupus erythematosus. 711 24


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