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)

Peripheral blood lymphocytes which contain and secret immunoglobulin were identified by fluorescent staining and a reverse hemolytic plaque assay. Significantly increased numbers of these cells were found in patients with active systemic lupus erythematosus compared with patients with rheumatoid arthritis, bacterial infections and normal controls. The increased numbers of these circulating activated B cells closely correlated with clinical and laboratory indices of disease activity, indicating their potential value in the management of lupus patients. However, the demonstration of pseudo-plaques in assays of lymphocytes from some lupus patients emphasizes the need to establish the true secreting nature of the plaques detected.
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PMID:Immunoglobulin-secreting cells in SLE: correlation with disease activity. 700 56

21 patients with criteria for systemic lupus erythematosus (SLE) and 12 normal controls were studied for their spontaneous circulating IgM and IgG plaque-forming cells (PFCs) reactive against sheep erythrocytes (SRBC) and against a panel of five haptens. Quantitatively defined active and mildly active SLE patients had significantly elevated IgM- and IgG-producing PFCs in their peripheral blood reactive with the panel of five chemically defined haptens. Those patients having inactive SLE also showed increased circulating IgM PFCs. Significant elevations in circulating hapten-reactive PFCs were found to correlate progressively with disease activity in the inactive, mildly active, and active SLE patient groups. Circulating IgM- and IgG-secreting PFC reactive against SRBC were both significantly elevated only in those patients with active SLE. The data support the concept that SLE patients have a generalized increase in B cell activity against a broad repertoire of determinants, even those ostensibly unrelated to natural tissue antigens.
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PMID:Increased multiclonal antibody-forming cell activity in the peripheral blood of patients with SLE. 702 41

Systemic lupus erythematosus (SLE) is characterized by increased numbers of circulating B cells activated polyclonally to secrete immunoglobulin. Because T cells secrete, or shed, various factors that are functionally important in regulating immunoglobulin production by B cells, a reverse hemolytic plaque assay was developed to quantitate such activated T cells. In this technique, we used a rabbit antiserum raised to supernatants of concanavalin-A--stimulated human lymphocytes. The relevant antigenic specificity of this antiserum is directed toward the shed surface membrane determinant(s) preferentially expressed on activated T cells. Freshly isolated peripheral blood mononuclear cells from 14 SLE patients contained more than 10 times the number of endogenously activated T cells than cells from normal subjects. Within the SLE group, plaque-forming T cells were particularly increased in patients with active disease. By linear regression analysis, a significant positive correlation was revealed between such activated T cells and immunoglobulin-secreting B cells, also measured by a reverse plaque assay (r = 0.83). It appears that both activated B cells and T cells circulate in increased numbers in SLE. Additional investigation will be required to define the molecular nature of the T cell product(s) being measured and to clarify the relationship of these findings to the immunoregulatory abnormalities in this disorder.
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PMID:Association between endogenously activated T cells and immunoglobulin-secreting B cells in patients with active systemic lupus erythematosus. 703 29

Normal human peripheral blood lymphocytes cultured in vitro with lupus sera (LS) were studied for their possible immunoglobulin (Ig) secretion using reverse haemolytic plaque assay (RHPA). Plaque forming cells (PFC) produced in cultures with LS (2,323 +/- 858 PFC/10(6) cultured cells) significantly increased in number compared to the control cultures with normal human serum (206 +/- 43, P less than 0.05). However, the artifactual nature of the PFC formation due to cytophilic Ig in LS subsequently became evident from the kinetic curves, trypsinization or medium change at the end of the culture period, radiation of cells on the first day of culture, or by depletion of nylon wool column-adherent cells from the culture system. These cytophilic Ig were observed in 56% of the sera obtained from untreated lupus patients. Thus, their possible interference with the resultant spurious plaque formation might be difficult to eliminate when performing RHPA in lupus patients.
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PMID:Pseudoplaque formation by cytophilic immunoglobulins in the sera of lupus patients as measured using reverse haemolytic plaque assay. 704 57

While attempting to evaluate CD5+ and CD5- anti-DNA-secreting plaque-forming cells (PFC) in patients with systemic lupus erythematosus (SLE), significant numbers of PFC against control sheep erythrocytes (ShE) treated with poly-L-lysine (PLL) but not further conjugated with single-stranded (ss) or double-stranded (ds) DNA were noted. Numbers of PFC obtained using PLL-ShE, ssDNA-ShE and dsDNA-ShE were not significantly different, all reactivity to DNA apparently being accounted for by binding of antibodies to PLL-treated ShE. Nevertheless, anti-PLL-PFC could be inhibited by soluble dsDNA included in the plaque assay. These findings might be explained by cationic anti-DNA antibodies binding non-specifically to anionic PLL. Control healthy subjects gave few PFC against PLL-ShE, ssDNA-ShE or dsDNA-ShE. Anti-PLL-PFC appeared to be related to disease activity, with higher numbers of both CD5+ and CD5- PFC in patients with clinically active SLE.
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PMID:CD5-positive and CD5-negative plaque-forming cells against poly-L-lysine-treated sheep erythrocytes in patients with systemic lupus erythematosus. 753 18

Although lupus vulgaris is the most common form of cutaneous tuberculosis seen in Europe, the incidence has steadily declined and it is now rarely seen. We report a case in a 69-year-old lady who presented with a 10-year history of a slowly growing plaque on the left cheek. Skin biopsy confirmed caseating granulomata, and acid-fast bacilli were seen. She was commenced on triple antituberculous therapy with good effect.
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PMID:Lupus vulgaris--a case report. 767 99

In western countries, acute myocardial infarction is the commonest cause of morbidity and mortality [19]. An occlusive coronary thrombus on an ulcerated atherosclerotic plaque in the coronary arteries is the etiological event in more than 90% of patients with Q-wave myocardial infarction [38]. The underlying abnormality in non-Q-wave myocardial infarction is often a ruptured atherosclerotic plaque, which acts as a nidus for the deposition and activation of platelets. In this case, thrombosis occurs, but may not be totally occlusive, or an early spontaneous recanalization may occur. On the other hand, some clinical trials showed that a prolonged treatment with antiplatelet drugs significantly reduces the recurrence of coronary ischemia. Thus, atherosclerosis is a necessary condition for myocardial infarction, but it is not sufficient in that it usually needs the occurrence of thrombosis. However, only 25-30% of these thrombotic events are prevented by the administration of antiplatelets drugs. In recent years, epidemiological studies identified some hemostatic parameters whose abnormalities may help predict the risk of ischemic events: fibrinogen [14], plasminogen activator inhibitor-1 (PAI-1) [3], lipoprotein(a) [46], anticardiolipin antibodies (ACA) and lupus anticoagulant (LA) [10], leukocyte count [34], blood viscosity [34]. Some of these, such as fibronogen and PAI-1 are acute-phase proteins.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma predictors of ischemic complications of atherosclerosis: open issues. 806 Dec 44

Despite an extensive literature dealing with IL2-induced cytolytic activity, noncytotoxicity-related effects of IL2 on peripheral blood mononuclear cells (PBMC) or T cell function have received less attention. We have focused on the effects of irradiated, IL2-activated PBMC (PBMC*rIL2) on anti-CD3- and formalin-fixed heat-killed Staphylococcus aureus-induced polyclonal B cell differentiation in secondary cultures. PBMC*rIL2 act directly on B cells and cross major histocompatibility complex barriers to augment polyclonal B cell differentiation as measured by plaque-forming cell (PFC) generation. These effects are preferentially mediated by T (both CD4+ and CD8+) cells, and physical contact between effector PBMC*rIL2 and target B cells is not absolutely required for enhanced PFC generation. PBMC*rIL2 must be present for the initial 24 hr of the secondary cultures, indicating that some soluble B cell differentiation factor rapidly released by PBMC*rIL2 mediates the PFC-enhancing effect. Of IL2, IL4, IL5, IL6, IL10, IFN-gamma, and TNF-alpha, only IFN-gamma mRNA is appreciably and reproducibly increased in irradiated, IL2-activated T cells (T cells*rIL2). Nevertheless, exogenous rIFN-gamma cannot mimic and anti-IFN antibodies cannot block the PFC-enhancing effects of T cells*rIL2, indicating that some unidentified soluble factor(s) apart from or in addition to IFN-gamma is involved. IL2-induced effects on T cell noncytolytic function may help explain certain observed immune anomalies in IL2-treated patients, and a better understanding of the IL2-induced effects on T cell noncytolytic function may have ramifications for autoimmune diseases such as SLE.
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PMID:Enhancing effects of interleukin 2-treated peripheral blood mononuclear cells on subsequent B cell differentiation. 806 23

A 40-year-old man presented with an ulcerated tumour in a fibrotic plaque on the dorsum of his left foot. Due to severe localized scleroderma, the patient had been treated with azathioprine 10 years earlier. Histopathology of the excised tumour revealed an anaplastic squamous cell carcinoma within a scar of localized scleroderma. The case demonstrates that not only patients with tense scar tissue following burning, congelation, chronic radiodermatitis, lupus vulgaris or lupus erythematosus but also patients who have had localized scleroderma may run a greater risk of developing squamous cell carcinoma. Immunosuppressive therapy has to be discussed as an additional risk factor in our patient. Therefore, narrow clinical follow-up was recommended for early detection of relapse.
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PMID:Squamous cell carcinoma in localized scleroderma following immunosuppressive therapy with azathioprine. 810 25

The family of antiphospholipid antibodies includes antibodies binding to cardiolipin in serological test for syphilis, antibodies prolonging the clotting time in lupus anticoagulant test, antibodies reacting with plasma phospholipid-binding proteins, such as beta 2-glycoprotein I and prothrombin, and antibodies binding to oxidized low-density lipoprotein (LDL). Antiphospholipid antibodies are traditionally associated with arterial and venous thrombosis in patients with primary or secondary antiphospholipid syndrome. The recent studies, especially those on patients with myocardial infarction, extend the concept of antiphospholipid antibodies, and suggest that they play a role also in atherosclerosis. Based on the clinical studies and immunological findings, it seems that the differences in the specificity of antiphospholipid antibodies may reflect to their pathogenetic mechanisms and, finally, to their clinical consequences. The present review suggests that antibodies to oxidized LDL may not interfere directly with blood coagulation, but seem to have importance in the inflammation of the vessel wall in atherosclerosis and in vasculitis. Instead, antibodies to beta 2-glycoprotein I and to prothrombin show a closer association with thrombosis. It is possible that in the atherosclerotic plaque, the plasma proteins, such as beta 2-glycoprotein I or prothrombin, are bound to the endothelial surface and antibodies to cryptic epitopes revealed in these proteins are induced. These antibodies may contribute to the formation of atherosclerotic thrombosis by changing the balance of haemostasis toward hypercoagulative state.
Lupus 1996 Oct
PMID:Antiphospholipid antibodies and atherosclerosis. 890 78


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