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)

Peripheral blood lymphocytes from patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), progressive systemic sclerosis (PSS), Reiter's disease, osteoarthritis, and from healthy volunteers were investigated for interferon-gamma (IFN-gamma) production after mitogen activation. Phytohaemagglutinin stimulation revealed an impaired IFN-gamma production in RA, SLE, and PSS but normal levels in Reiter's disease and osteoarthritis. In RA this deficiency was also seen after pokeweed mitogen, OKT3, and concanavalin A activation. No major differences were found in interleukin 2 (IL-2) production and cell proliferation. The IL-2 receptor expression was reduced on stimulated RA lymphocytes. The deficient IFN-gamma production was compensated in RA by co-stimulation of PHA or OKT3 with phorbol myristic acetate (PMA). In addition, the combination of the calcium ionophore A 23187 and PMA induced a strong IFN-gamma secretion in all patient groups and in the controls.
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PMID:Impaired mitogen-induced interferon-gamma production in rheumatoid arthritis and related diseases. 312 62

A low natural killer (NK) activity has been well documented for lymphocytes from systemic lupus erythematosus (SLE) patients. Given the defect in interferon-gamma (IFN-gamma) and interleukin 2 (IL-2) production also reported in SLE, it seemed possible that the absence of these molecules could account for some of the defective NK activity. We have tested the NK activity present in peripheral blood mononuclear cells (PBMC) from SLE patients and its in vitro modulation by different preparations of exogenous IL-2. We have found a low NK activity for PBMC from steroid-treated SLE patients, and we report an enhancement in lytic activity after incubation with mitogen-induced, IL-2-containing supernatants obtained from human tonsils. This increase did not seem to be due to recruitment of new effectors because the numbers of cells expressing NK phenotype (Leu 7+ or Leu 11b+) did not change after the incubation, nor did the target specificity of the lysis. However, a similar degree in the improvement in cytotoxicity was not obtained by incubation with a purified preparation of IFN gamma and/or recombinant IL-2 (rIL-2). A possible role for a molecule other than these lymphokines that might influence this effect is discussed.
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PMID:Role of interleukin 2 in inducing normalization of natural killer activity in systemic lupus erythematosus. 313 45

The production of interferon (IFN) by peripheral blood lymphocytes from patients with rheumatoid arthritis (RA) and of IFN and interleukin 2 (IL-2) in systemic lupus erythematosus (SLE) was compared with that of healthy controls. Patients with SLE showed a significant reduction in IL-2 production compared to controls if the PBL were irradiated before mitogen stimulation. No patient with RA or SLE studied had impaired IFN production regardless of disease activity and the IFN produced was always IFN-gamma in type. We conclude that there is an abnormality in IL-2 production in SLE but there is no abnormality in IFN-gamma production in either RA or SLE.
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PMID:Lymphokine production in rheumatoid arthritis and systemic lupus erythematosus. 314 12

The autologous mixed lymphocyte reaction (AMLR) represents the activation, proliferation and differentiation of T cells in response to signals from autologous non-T cells. Upon stimulation by autologous non-T cells, OKT4+ cells produce interleukin 2 (IL2); cells contained within both OKT4+ and OKT8+ cell populations can also be activated by autologous non-T cells to become sensitive to IL2. Once these activated OKT4+ and OKT8+ cells are exposed to IL2 produced by OKT4+ cells, they will proliferate and go on to differentiate into effector cells. Patients with systemic lupus erythematosus (SLE) have a defect in the AMLR. The ability of OKT4+ cells to produce IL2 in the AMLR is impaired. Upon triggering with autologous non-T cells, their OKT8+ cells become sensitive to proliferative signals of IL2; however, their OKT4+ cells fail to express IL2 receptors. These defects are a consistent feature in patients with SLE. AMLR-induced immunologic processes which require cell interactions between OKT4+ cell subpopulations are not correctable even by the addition of normal IL2. However, the immunologic processes mediated through OKT4+-OKT8+ cell interactions can be corrected with normal IL2. The latter finding suggests that the partial correction of the AMLR-induced immunologic processes with IL2 might lead to suppressed B cell hyperactivity of patients with SLE.
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PMID:Abnormalities in autologous mixed lymphocyte reaction-activated immunologic processes in systemic lupus erythematosus and their possible correction by interleukin 2. 315 46

Systemic lupus erythematosus (SLE) is characterized by multiple T and B cell abnormalities. This study was designed to investigate the cell surface membrane characteristics of T cells by using single and double immunofluorescence and examine the role of HLA-DR+ T cells in the production of immunoglobulin by B cells. The results presented: (a) confirm the presence of a larger population of T-cells bearing DR antigens in patients with SLE than in normal controls, (b) demonstrate that DR positive cells are equally distributed in helper/inducer and suppressor/cytotoxic subsets of lymphocytes from patients with SLE, (c) show no elevation in the percentage of T cells bearing interleukin 2 (IL-2) receptors, (d) demonstrate that DR positive, but not DR negative T-cells, multiply in the presence of conditioned media and, (e) demonstrate that DR positive T cells provide helper factors which enhance the production of immunoglobulin by B cells. We propose that T-cells bearing DR antigens in patients with SLE are functional in vivo, and may be responsible for the B cell overactivity.
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PMID:Activated T lymphocytes in the peripheral blood of patients with systemic lupus erythematosus induce B cells to produce immunoglobulin. 326 40

Three strains of mice bearing the autosomal recessive lpr gene (MRL, C57BL/6, and C3H) that had spontaneously developed a lupus-like disease were studied sequentially for functional natural killer (NK) and natural cytotoxic (NC) cell activity. Natural killing was impaired in spleen and bone marrow cells from all the lpr strains, as well as from the congenic strain MRL--+/+, which develops a late onset lupus-like disease. The NK cell activity was found to be depleted as early as 2 months of age in all lpr strains, and decreased further with age. NK activity was augmentable by Poly I:C and interleukin 2 (IL-2), suggesting that the residual cells can respond to NK modulators. In contrast with NK cell activity, NC activity was not decreased in lpr mice but could be augmented by IL-3-rich supernatants. The spontaneous decrease in NK cell activity was associated with an increased autologous plaque-forming cell (APFC) response to bromelin-treated mouse red blood cells, which is produced primarily by B cells possessing the Ly-1 phenotype (Lyt-1+ B). When NK cell activity was increased by exogenous administration of Poly I:C, the APFC response diminished. Treatment of spleen cells with anti-asialo GM1 prior to Poly I:C treatment resulted in a decreased NK response but increased both APFC and Lyt-1+ B cells. The possible regulation of autoreactivity by NK cells is discussed.
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PMID:Altered natural killer and natural cytotoxic cellular activities in lpr mice. 348 60

To investigate the role of interleukin 2 (IL-2) in systemic lupus erythematosus (SLE) mononuclear cells (MNC) of 68 SLE patients were tested for their ability to produce and also to respond to IL-2. Cells were collected monthly over an one year period. IL-2 production by MNC was measured under various conditions after optimal and suboptimal stimulation. Although we found a large variation in IL-2 production by individual MNC preparations no statistical significant differences were found between normal and SLE cells. To study IL-2 responsiveness, proliferation of MNC was studied under conditions where endogenous IL-2 production is limiting. Addition of IL-2 resulted in a four- to eight-fold enhancement of proliferative responses. However also in this respect no differences were found between SLE patients and healthy controls. Thus, in this group of SLE patients no abnormalities in IL-2 production or response could be demonstrated.
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PMID:T cell function in systemic lupus erythematosus: normal production of and responsiveness to interleukin 2. 348 49

To study the mechanisms that regulate the activity of interleukin 2 (IL 2) and possibly limit its activity, we have examined normal human serum for its ability to inhibit IL 2-mediated proliferation of a cloned IL 2-dependent cytotoxic T lymphocyte line (CTLL). Normal human serum contains a factor capable of inhibiting IL 2 dependent proliferation of CTLL cells. This factor is absorbed with the cells but not IL 2 molecules. The inhibitor is heat-labile and inactivated by trypsin treatment. The molecular weight of the inhibitor is 70,000-220,000. The imbalance of the inhibitor is observed in serum from patients with autoimmune disease including systemic lupus erythematosus and rheumatoid arthritis. These results suggest that the serum IL 2 inhibitor may play an important role in the in vivo regulatory mechanism of IL 2 activity and in aberrant immune functions in humans.
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PMID:Inhibition of interleukin 2 by serum in healthy individuals and in patients with autoimmune disease. 349 91

To determine whether patients with systemic lupus erythematosus (SLE) and active nephritis have more profound defects in cell-mediated immunity (CMI), we studied T-colony-forming cells (TCFC) in 12 patients with lupus nephritis (LN) and 14 patients with chronic mesangial proliferative glomerulonephritis (CGN) without renal insufficiency. We also examined the activity of T-colony-stimulating factor (TCSF) in media conditioned by phytohaemagglutinin (PHA) stimulated peripheral blood lymphocytes (PHA-LCM). The levels of TCFC and TCSF were decreased in patients with LN compared with those in normal controls and lower in LN patients with the nephrotic syndrome (NS) than in those without NS. In contrast, these CMI parameters in CGN patients with or without NS did not differ from normal subjects. TCSF activity for TCFC in both normal individuals and LN patients was removed from PHA-LCM with interleukin 2 (IL 2) receptor bearing cultured T cells. These in vitro findings suggest that IL 2 is the essential factor contained in PHA-LCM. Our observations may lend further insight into the understanding of the immunoregulatory defect in LN.
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PMID:Defective T-lymphocyte colony formation in patients with lupus nephritis. 350 75

The lymphokine, interleukin 2 (IL-2), is an important modulator of cell-mediated immune (CMI) responses. We report here the detection of an inhibitor of IL-2 in normal sera by measuring the inhibition of thymidine incorporation in IL-2 dependent murine CTLL cells. The inhibitor, partially purified by Sephacryl S-200 gel filtration, eluted with the 60,000-70,000 mol. wt fraction. The factor was destroyed at 56 degrees C for 30 min and did not bind to Protein A Sepharose, suggesting that it is not an immunoglobulin G. Of 26 normal sera tested, 23 had significant levels of the inhibitor. Since connective tissue diseases are often associated with deficient CMI responses, we examined the levels of IL-2 inhibitor in 26 systemic lupus erythematosus (SLE) and 22 rheumatoid arthritis (RA) patients. Only 8 SLE and 12 RA patients had normal levels of the inhibitor. Of the 18 SLE patients with low or undetectable levels, 15 had clinically defined active disease and of the eight with normal levels, three had active disease. The decrease in the IL-2 inhibitor level did not correlate either with steroid or cyclophosphamide treatment or with serum levels of DNA binding and C3. These data suggest that the function of the inhibitor is to control IL-2 activity under normal conditions. Decreased levels of the IL-2 inhibitor in these patients might be explained either as a reduced requirement of this regulatory protein secondary to decreased IL-2 production or a defect of the cells responsible for the production of both IL-2 and its inhibitor.
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PMID:Decreased interleukin 2 inhibitor in sera of patients with autoimmune disorders. 379 99


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