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)

Immunological dysregulation is an important cause of the development of systemic lupus erythematosus (SLE). Serological evaluation has been useful in the clinical management of patients and as a prognostic indicator. Sixteen patients who developed SLE as children were followed up for more than three years and immunological data collected. The results showed that (a) complement C3 concentration was lower in the active stage of SLE, especially during a major clinical exacerbation, but rarely preceded a major flare up. The concentration was often normal during the mildly to moderately active stage. In contrast, a low complement C4 concentration often preceded a major clinical exacerbation and could be of longer duration, sometimes persisting regardless of disease activity. (b) A T cell subset distribution study showed persistently low CD4 positive T cells in the peripheral blood of patients with SLE during the long term follow up, strongly suggesting that the intrinsic defect is mainly localised in T helper/inducer cells. These abnormal cellular defects did not tend to return to normal even in long term remission. (c) The persistently higher serum interleukin 2 and interleukin 2 receptor concentrations in SLE strongly suggested that the T cells were preactivated in vivo and that these phenomena might persist even in remission. (d) The best single parameter for predicting active SLE was anti-dsDNA. It was highly correlated with disease activity in most patients, and the asymptomatic increase of anti-dsDNA (greater than or equal to 60 U/ml, radioimmunoassay) was often followed by a major clinical exacerbation, especially in patients with a simultaneously low complement C4 concentration, suggesting that it might be an important warning sign of a major flare up. High dose steroids are indicated in this group of patients.
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PMID:A long-term immunological study of childhood onset systemic lupus erythematosus. 154 37

Skin biopsy specimens from nine patients with lupus vulgaris were examined in situ by means of monoclonal antibodies directed against phenotypes of lymphocyte subsets, Langerhans cells, HLA-DR antigens, and interleukin 2 receptor. The epidermis showed prominent changes, including intense expression of HLA-DR on keratinocytes, increase in epidermal cell layers, moderate to high Langerhans cell hyperplasia, and infiltration by CD3+ pan-T cells as well as CD8+ (cytotoxic/suppressor) and CD4+ (helper/inducer) T cells. The predominant lymphocyte in the dermal granulomas was the activated CD3+ T cell, expressing major histocompatibility complex class II antigens and interleukin 2 receptor. CD4+ and CD8+ cells were randomly distributed among the epithelioid cells, which showed intense staining for major histocompatibility complex class II antigens. In all except two patients, the CD4+ population was greater than that of the CD8+ cells. CD1+ Langerhans cells were scattered in moderate numbers in the dermal granulomas. Acid-fast bacilli were conspicuously absent in the biopsy specimens. These features suggest that T-cell activation and Langerhans cell hyperplasia are prominent features of dermal tuberculosis.
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PMID:In situ characterization of cellular infiltrates in lupus vulgaris indicates lesional T-cell activation. 168 89

Serum soluble interleukin 2 receptor (sIL2R) was measured in patients with active and inactive systemic lupus erythematosus (SLE). The concentration of sIL2R was higher in inactive SLE than in normal controls and was significantly increased in active compared with inactive SLE. When patients with active SLE were followed up serially it was found that the sIL2R concentration fell when the disease became inactive. There was no statistically significant association between sIL2R and the grades of disease activity, however. In patients with either active or inactive SLE and infection the sIL2R concentration was much higher than in those without infection. Chronic infection (tuberculosis or candida) was associated with a much higher concentration of sIL2R than pyogenic or herpes zoster infection. The sIL2R concentration helps to distinguish infection in patients with SLE.
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PMID:Serum soluble interleukin 2 receptor in systemic lupus erythematosus: effects of disease activity and infection. 195 94

We studied 10 patients with thrombotic thrombocytopenic purpura (TTP) and 5 patients with hemolytic uremic syndrome (HUS). Common cold symptoms were observed in 2 with TTP and 3 with HUS, and SLE was noted or suspected in 3 with TTP, and the onset was after operation in on with TTP and one with HUS. All TTP patients had coma and high fever. Renal failure was noted in 3 with TTP and their prognosis was poor. Seven patients with TTP and 4 patients with HUS survived. Autoantibody was highly positive in TTP but slightly positive in HUS. High molecular weight multimer of von Willebrand factor was decreased in 3 of 6 with TTP, platelet aggregating factor was positive in 4 of 6 with TTP, and microthrombus was observed in 7 of 8 with TTP. Tumor necrosis factor was increased in 5 of 9 with TTP and HUS, Interleukin-1 beta was increased in all TTP and HUS patients, and soluble interleukin 2 receptor and interferon alpha were also increased. Although plasma exchange was generally effective, some patients required combination therapy with steroids. We speculated that an autoimmune mechanism was involved in the on onset of TTP.
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PMID:[Clinical analysis on thrombotic thrombocytopenic purpura and hemolytic uremic syndrome, with plasma level of cytokine]. 224 29

Lymphocytes upon activation release a soluble form of interleukin 2 receptor (IL-2R). Systemic autoimmune disorders are characterized by immune system disregulation associated with cellular activation; therefore we sought to determine the levels of soluble IL-2R molecules in the serum of patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and primary Sjogren's syndrome (1 degree SS). Utilizing an enzyme immunoassay method we found increased serum levels of soluble IL-2R in 65.4% (34/52) of RA, in 34.9% (15/43) of SLE, and in 25.0% (13/52) of 1 degree SS patients, compared to 4.2% (1/24) of healthy individuals. High serum levels of soluble IL-2R correlated with several indices of disease activity in RA and SLE patients, as well as with disease progression to extraglandular involvement and to pseudolymphoma or lymphoma in patients with 1 degree SS. By gel filtration analysis, the soluble IL-2R circulating in the serum of a RA patient corresponded to a high molecular weight molecule (greater than 90 kDa) compared to the 65-kDa soluble IL-2R molecule released by phytohemagglutinin-stimulated normal peripheral lymphocytes.
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PMID:Soluble interleukin 2 receptor molecules in the serum of patients with autoimmune diseases. 278 95

The concentration of soluble interleukin 2 receptor (IL-2R) was determined in the serum of 54 patients with systemic lupus erythematosus (SLE) by an enzyme linked immunosorbent assay (ELISA) using two monoclonal antibodies with the IL-2R. Concentrations of soluble IL-2R in the serum of the patients with SLE (study group) were significantly higher than in 20 normal subjects (control group). The relation between concentrations of soluble IL-2R and clinical findings was investigated. The concentration of soluble IL-2R showed no particular relation with the clinical manifestations and did not correlate with the level of anti-DNA antibody or CH50. Significant correlation between the concentration of soluble IL-2R and disease activity did exist, however. Furthermore, the concentration of soluble IL-2R in some cases changed simultaneously with the disease activity. Thus the concentration of soluble IL-2R may serve as a new clinical indicator of disease activity in patients with SLE.
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PMID:Relation between soluble interleukin 2 receptor and clinical findings in patients with systemic lupus erythematosus. 281 16

Sera obtained from patients with systemic lupus erythematosus (SLE) were tested for their reactivity to cell lines derived from cutaneous T-cell lymphoma (CTCL), or adult T cell leukaemia (ATL), and with other cell lines, by indirect immunofluorescence method. Approximately one half of SLE sera reacted with the surface antigens of HUT-102 cells, a cell line from CTCL, which constitutively expresses Tac antigen. The titre tended to be higher in the active than in the inactive stage. These positive sera also reacted with other neoplastic or normal T cell lines having Tac antigen. SLE sera reacting with HUT-102 surface antigens were further examined for their reactivities to Tac antigen, the putative IL-2 receptor, using HUT-102 or ATL-2. Pretreatment with anti-Tac monoclonal antibody partially blocked the reactivities to HUT-102 surface antigens in nine of 15 SLE sera tested. The binding of 125I-labelled anti-Tac monoclonal antibody was displaced by the addition of sera from six of 15 SLE patients. In addition, nine of the 15 SLE sera could inhibit the binding of 125I-labelled IL-2 to ATL-2 cells. These results suggested that some of SLE sera contained antibodies against the IL-2 receptor.
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PMID:Systemic lupus erythematosus sera antilymphocyte reactivity: detection of antibodies to Tac-antigen positive T cell lines. 300 53

Mice homozygous for the lpr gene spontaneously develop massive lymphoproliferation and an associated lupus-like autoimmune disease. In addition, the total lymphoid organs from these mice express high levels of mRNA for the c-myb proto-oncogene. Since enhanced c-myb mRNA is normally observed in immature thymic lymphocytes but not normal peripheral T cells, this may be indicative of the abnormal maturation state of lpr T lymphocytes. To determine whether the abnormal Lyt-2-, L3T4- (double negative) T lymphocytes in lpr mice express high c-myb, we purified this population by complement-mediated lysis with anti-L3T4 and Lyt-2 antibody from B6/lpr lymph nodes. We found that increased c-myb mRNA is expressed by this double-negative subset. To assess whether the high level of c-myb correlated with the aberrant undifferentiated state of these cells, we examined the effects of T cell differentiation inducers, phorbol ester and calcium ionophore, on c-myb expression. We found that c-myb levels were depressed after phorbol ester and calcium ionophore treatment. Concomitantly, transcriptional activation of the interleukin 2 receptor gene and progression of these cells through the cell cycle were observed. Thus, in B6/lpr double-negative T cells, the regulation of c-myb, interleukin 2 receptor, and cell proliferation may be interrelated. A combination of Northern hybridization and nuclear run-on transcription assays revealed two levels at which c-myb can be regulated in the double-negative T cell subset. The gene is transcriptionally regulated in untreated cells, but on induction with phorbol ester and calcium ionophore, the gene is negatively regulated via post-transcriptional mechanisms.
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PMID:The expression and regulation of c-myb transcription in B6/lpr Lyt-2-, L3T4-T lymphocytes. 311 95

In order to assess the importance of interleukin 2 receptor (IL-2R)-positive activated lymphocytes and macrophages in the pathogenesis of autoimmunity, we tested the prophylactic therapeutic efficacy of an anti-IL-2R (M7/20) monoclonal antibody, which recognizes the 55-kDa subunit of the heterodimeric IL-2R in two distinct models: the nonobese diabetic mouse and the NZB x NZW F1 hybrid with lupus. Treatment with anti-IL-2R monoclonal antibody suppressed autoimmune insulitis in nonobese diabetic mice and lupus nephritis in the NZB x NZW F1 hybrid. These studies indicate that highly selective targeting to activated lymphocytes and macrophages expressing the IL-2R provides a discrete method of dampening autoimmunity.
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PMID:Anti-interleukin 2 receptor antibody suppresses murine diabetic insulitis and lupus nephritis. 312 42

The objective of this study was to define immunologic T cell abnormality characteristic of active systemic lupus erythematosus (SLE). Eight of nine patients who had severe clinical and laboratory manifestations of active SLE had a characteristically marked increase in OKT4+ and a decrease in OKT8+ T cells. Using OKIa1 and OKDR monoclonal antibody, we found that, in circulating blood of all patients with active SLE, an increased percentage of Ia+ and DR+ T cells is present compared to inactive SLE. Five of these active SLE patients had Tac+ antigens, an interleukin 2 receptor on OKT4+ and OKT8+ T cell subsets in resting blood. The present study demonstrates that Ia+ and DR+ antigens are selectively expressed on the majority of OKT4+ T cell subsets of all patients with active SLE, whereas Ia+ and DR+ antigens are expressed almost equally on both OKT4+ and OKT8+ T cell subsets in inactive SLE. The elevated percentage of Ia+, DR+, OKT4+ T cells in active SLE was accompanied by a highly depressed proliferative response to T cell mitogens, phytohemagglutinin and concanavalin A. However, OKT8+ T cell subsets in active SLE possessed a normal proliferative response to these T cell mitogens. We conclude that this abnormality of activated OKT4+ T cells bearing HLA-DR antigens may play a role in the development of active SLE.
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PMID:OKT4+ T cell abnormality in patients with active systemic lupus erythematosus: HLA-DR antigen expressions. 326 Jan 61


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