Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antinuclear antibodies can give diagnostic informations according to their titre values, the belonging to different classes of immune globulins and on the basis of different patterns of immunofluorescence connection. The determination of granulocyte-specific antibodies which frequently appear in progressive chronic polyarthritis further contributes to the differential-diagnostic classification of diseases of the connective tissue. An antibody against extractable nuclear antigen is specific for the so-called mixed connective tissue disease, an antimitochondrial antibody for the pseudo-LE-syndrome. Moreover, the own examinations resulted in a particularly high and frequent ability of complement fixation of the antinuclear factors in systematic lupus erythematosus and sclerodermy. In contrast to this in the progressive chronic polyarthritis the complement fixation was clearly more insignificant.
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PMID:[Possibilities of differentiation of antinuclear antibodies]. 76 33

A profound defect in granulocyte chemotaxis was documented in an otherwise healthy 21-yr-old man who failed to localize granulocytes to an area of cellulitis during an allergic reaction to cephalothin. During the period of drug allergy, characterized by urticaria, eosinophilia, and profound hypocomplementemia, in vitro migration of the patient's granulocytes in the Boyden chamber was markedly impaired. Although devoid of hemolytic complement activity, the patient's serum possessed supranormal chemotactic activity, even following heat inactivation, suggesting the presence of chemotactically active complement split products. Chemotactic function improved concomitantly with steroid therapy and normalization of serum complement levels, and was entirely normal following clinical recovery and cessation of steroid therapy. The chemotactic abnormality noted in the patient's cells was reproduced in normal granulocytes by preincubation either with patient serum or with cobra venom-activated fresh (but not heated) normal serum, suggesting that in vivo exposure of granulocytes to activated complement was responsible for the patient's abnormal chemotactic response. This mechanism may contribute to the increased infection propensity noted in other conditions characterized by in vivo complement activation, such as rheumatoid arthritis and systemic lupus erythematosis.
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PMID:Acquired granulocyte abnormality during drug allergic reactions: possible role of complement activation. 83 Mar 75

The concentration of granulocyte elastase-alpha-1-protease inhibitor (E-AT) complex in plasma is enhanced in inflammatory processes, e.g. in septicaemia and rheumatoid arthritis, being an expression of granulocyte activation during inflammatory response. In the present study we measured E-AT and fibronectin in the plasma of 46 patients with various connective-tissue diseases in relation to the course of the disease. In about 50% of the cases, E-AT was found to be elevated to 2-3 times the normal concentrations, in relation to increasing serum content of C-reactive protein. In follow-ups over 2 years, an elevation of E-AT and a decreasing fibronectin in plasma was found in patients with activated disease. Without relation to other parameters used in connective-tissue diseases, fibronectin was found to be diminished below the normal range in 7 patients with systemic lupus erythematodes and 1 patient with overlapping syndrome. Our results indicate that the concentration of E-AT and fibronectin in plasma may be helpful parameters for judging the activity of connective-tissue diseases.
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PMID:Concentration of fibronectin and granulocyte elastase in plasma of patients with systemic connective-tissue diseases. 349 2

We applied a radiolabeled antiglobulin test to a study of patients with a variety of neutropenic disorders. After defining the nature of the interaction of radiolabeled anti-IgG with the neutrophil, we studied 16 patients with neutropenia of uncertain etiology and adequate bone marrow granulocyte precursors. Twelve of these 16 patients had increased neutrophil-associated IgG (PMN-IgG). Patients with the highest levels of PMN-IgG had the lowest neutrophil counts. The majority of patients with neutropenia and increased PMN-IgG had an underlying immunologic disorder that included immune thrombocytopenic purpura in 5 patients and autoimmune hemolytic anemia in 1 patient. In some patients, elevated PMN-IgG preceded other evidence for immunologic disease. The direct antiglobulin test helped to distinguish neutropenic patients with increased PMN-IgG both from patients with neutropenia due to a known nonimmune disorder and from nonneutropenic patients with rheumatoid arthritis or systemic lupus erythematosis. Each of four patients with increased neutrophil-associated IgG treated with systemic corticosteroids responded clinically with an associated fall in neutrophil IgG and a rise in the circulating neutrophil count. The radiolabeled antiglobulin test appears useful in defining a subpopulation of patients with neutropenia due to an underlying immunologic disorder.
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PMID:Granulocyte-associated IgG in neutropenic disorders. 697 94

The expression of adhesion molecule Leukocyte Function Antigen-1 (LFA-1) on peripheral blood leukocytes was evaluated (using a monoclonal antibody anti CD11a/LFA-1) in 52 spondylarthropathies (SA) (35 HLA B27 positive), 12 healthy patients, 24 active rheumatoid arthritis (RA) and 12 systemic lupus (SLE) patients. LFA-1 expression on lymphocytes was similar in the different groups of patients, but LFA-1 expression on granulocytes was higher in SA than in controls (p < 0.05) or in RA or SLE. Fluorescence intensity of anti LFA-1 staining on SA granulocytes correlated with serum IgA levels. There was no difference between HLA B27 positive/negative, biologically inflammatory (CRP > 21 mg/l)/non inflammatory SA patients. This study seems to confirm the granulocyte and IgA involvement in immunopathogenesis of spondylarthropathies.
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PMID:[Leukocyte expression of the LFA-1 adhesion molecule in spondylarthropathies]. 800 Mar 97

We have studied the ability of the lupus prone MRL lpr/lpr (MRL/lpr) and (NZBxNZW)F1 (NZB/W) female mice to raise granulocyte mediated inflammatory responses. These autoimmune strains, known to exhibit severe anergy as concerns T cell dependent immune function, are not well analysed with respect to neutrophil-mediated inflammatory responses. An in vivo model of granulocyte mediated inflammation has been developed in our laboratory. A single intradermal injection of olive oil into mouse footpad induces massive infiltration of polymorphonuclear cells (PMNC) within 24 h. This extravasation of PMNC gives rise to a localized footpad swelling, which can be easily and reproducibly measured and relates to severity of the inflammatory process. T cell independence of this inflammatory model was ascertained by in vivo T cell depletion using monoclonal antibodies to CD4 and CD8 molecules. Olive oil triggered inflammation was inducible in both young and aged lupus mice. The intensity of footpad swelling upon olive oil injection was similar in lupus mice and in healthy control strains. In contrast, aged MRL/lpr and NZB/W mice showed severely depressed T cell dependent inflammatory responses as assessed by delayed type hypersensitivity reaction to sheep red blood cells. We conclude that the PMNC mediated inflammatory potential is not affected in severely diseased lupus mice. The increased numbers of circulating PMNC together with intact PMNC function may explain why severely immune deficient lupus mice seldom show clinical signs of bacterial infection.
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PMID:Neutrophil mediated inflammatory response in murine lupus. 832 62

Murine lupus and the analogous human disease systemic lupus erythematosus (SLE) in humans are characterized by multisystem disease accompanied by the production of numerous serum autoantibodies. The classic model of murine lupus is the New Zealand black mouse (NZB). In this strain anti-DNA antibodies are the most specific marker for the presence of murine lupus, in that this autoantibody parallels both the development and activity of the disease. Exposure to ultraviolet (UV) radiation is known to exacerbate the disease in both the murine and the human disease. UV irradiation of the skin increases serum levels of certain cytokines including interleukin-1 (IL-1), IL-6, and granulocyte/macrophage-colony stimulating factor (GM-CSF), which can influence B- and T-cell function. Recent studies have focused on the role of cytokines in SLE. We hypothesize that the ultraviolet (UV)-induced exacerbation in NZB mice in part is mediated by UV-induced cytokines such as IL-1. Eight-week-old female NZB and DBA/2 mice were exposed to UV irradiation. Sera and supernatants from spleen cell cultures were assayed for anti-DNA antibodies. After UV exposure, NZB mice showed a marked increase in such antibodies. Skin from both strains of mice was probed for IL-1 alpha mRNA before and after UV irradiation. At 24 h, DBA/2 mice had a slight increase in mRNA coding for IL-1 alpha, whereas a much greater increase in skin IL-1 alpha was seen in the NZB skin. This increase in IL-1 mRNA was associated with similar increases in IL-1 bioactivity. These data suggest that the mechanism underlying the UV-induced exacerbation of lupus is mediated in part by the cutaneous production of IL-1.
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PMID:Epidermal cytokines in murine lupus. 842 94

Calprotectin (L1) is a granulocyte and monocyte cytosolic protein released during activation of these cells. The plasma level of L1 has been shown to be a good marker of disease activity in rheumatoid arthritis. In this cross-sectional study of 100 patients with systemic lupus erythematosus (SLE), the serum level of L1 was found to be higher in patients than in matched controls (3661 micrograms/l versus 1051 micrograms/l; P < 0.001). The serum level of L1 was the only laboratory parameter with significant association to the disease activity index SLEDAI (r = 0.28; P < 0.01). Furthermore, the serum level of L1 was significantly higher in SLE patients with anti-DNA antibodies compared to patients without anti-DNA antibodies (4501 micrograms/l versus 3279 micrograms/l; P = 0.01). SLE patients with arthritis had higher serum levels of L1 than patients without arthritis (7652 micrograms/l versus 2811 micrograms/l; P < 0.01), indicating that the serum level of L1 also reflects arthritis activity in SLE.
Lupus 1993 Feb
PMID:Calprotectin in patients with systemic lupus erythematosus: relation to clinical and laboratory parameters of disease activity. 848 59

Nine patients with SLE-associated neutropenia and infections received 48 Mio U G-CSF per day s.c. for 2-17 days as an adjunct to antibiotic treatment. Granulopoiesis was normal or hyperplastic in all cases. The mean granulocyte count increased within 2 days from 1.4 per nl to 11.4 per nl. Side-effects were exacerbating CNS symptoms in two patients and a case of leukocytoclastic vasculitis. G-CSF induced constantly a rapid and distinct increase of neutrophil granulocytes in lupus-associated neutropenia patients with normo- or hyperplastic granulopoiesis.
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PMID:[G-CSF in patients with lupus-associated neutropenia and infections]. 876 47

Monocytes/macrophages activated by Th1 stimulation such as interferon-gamma (IFN-gamma) and CD40 ligand (CD40L) infiltrate the kidney and play a critical role in the progression of lupus nephritis (LN). We examined the monocyte response to Th1 stimulation and their effector function toward activating renal resident cells in patients with LN. Following stimulation with IFN-gamma granulocyte macrophage-colony stimulating factor (GM-CSF)/recombinant CD40L the production of tumor necrosis factor-alpha and IL-12 p70 by PBMC was significantly higher in LN patients. In coculture experiments employing activated monocytes and human mesangial cells, there was a trend toward higher monocyte chemoattractant protein-1 production by lupus monocytes compared to normal controls. Basal expression of CD40, ICAM-1, and STAT-1 was significantly higher in monocytes from LN patients, suggesting ongoing activation. Monocyte response to IFN-gamma, as accessed by intercellular adhesion molecule-1 upregulation and phosphorylation of STAT-1, was comparable between the two groups. Thus, in contrast to earlier reports, Th1-dependent monocyte activation is not impaired. In this disease activated monocytes appear to be fully capable of inducing renal injury.
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PMID:Monocyte response to Th1 stimulation and effector function toward human mesangial cells are not impaired in patients with lupus nephritis. 1258 53


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