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)

Antiphospholipid syndrome (APLS) is characterized by thrombocytopenia, thromboembolic phenomena and recurrent fetal loss, associated with anti-cardiolipin antibodies (ACA) and/or lupus anticoagulant. The syndrome may be primary or may be associated with other conditions such as systemic lupus erythematosus (SLE). In this study we induced primary APLS following immunization of BALB/c mice with a human monoclonal ACA (H-3). Analysis of the cytokine profile of the mice with experimental APLS indicated low production of IL-2, IL-3 and granulocyte-macrophage colony-stimulating factor (GM-CSF) by concanavalin A (Con A)-stimulated splenocytes of H-3 immunized mice. It seems that the low levels of IL-3 and GM-CSF have a potential role in the fetal loss of the APLS. Whatever the mechanism of IL-3 and GM-CSF in preventing fetal loss, these results may have therapeutic bearing on the reproductive outcome in women and other species with APLS.
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PMID:The putative role of cytokines in the induction of primary anti-phospholipid syndrome in mice. 142 85

Antiphospholipid syndrome (APLS) is characterized by thrombocytopenia, thromboembolic phenomena, and recurrent fetal loss, associated with anticardiolipin antibodies (ACA) and/or lupus anticoagulant. The syndrome may be primary or may be associated with other conditions such as systemic lupus erythematosus. We have previously shown the ability to induce APLS in naive mice following passive transfer of serum and monoclonal ACAs. Similarly we generated the secondary APLS in BALB/c mice following immunization with a pathogenic anti-DNA antibody. In the current study we report on the induction of primary APLS following immunization of BALB/c mice with a human monoclonal ACA (H-3). The mice developed high persistent titers of ACA. The APLS was characterized by prolonged activated partial thromboplastin time, low fecundity rate (21% vs. 48% of control immunized mice), high resorption index of fetuses (25% vs. 3%), and low weights of embryos and placentae. Our study points to the ability of inducing primary APLS in naive mice. The induction of various presentations of APLS by different ACA may explain the diversity of clinical manifestations seen in patients with APLS.
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PMID:Induction of primary antiphospholipid syndrome in mice by immunization with a human monoclonal anticardiolipin antibody (H-3). 156 94

A new fluorimetric assay was used to measure the relative amounts of antibodies to individual nuclear histones in sera from 102 patients with systemic lupus erythematosus (SLE), mixed connective tissue disease, primary sicca syndrome, and rheumatoid arthritis with vasculitis. In SLE sera, the predominant responses were to histones H-1, H-2B, and H-3, with marked elevations of binding to H-1 and H-2B in one-third of the patients, and to H-3 in one-fourth; antibodies of both the IgG and IgM classes were also detected. In a few SLE sera, the pattern of histone response differed or was restricted to 1 immunoglobulin class. In mixed connective tissue disease, only 2 of 9 sera showed elevated histone binding activity, the response being predominantly to H-3 in 1 patient and to H-1 and H-2B in the other. Binding to H-2B was also prominent in 2 of 3 patients with primary sicca syndrome. The highest antihistone reactivity and the most heterogeneous response patterns were observed in patients who had rheumatoid arthritis with vasculitis; 6 of 8 of those sera had elevated histone reactivity. In SLE, the highest histone binding results were found among patients with a history of photosensitivity. Histones are closely associated with DNA in the nucleosome, and we speculate that antihistone antibodies could arise as a result of damage to DNA, induced by drugs or irradiation.
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PMID:Patterns of antihistone antibody specificity in systemic rheumatic disease. I Systemic lupus erythematosus, mixed connective tissue disease, primary sicca syndrome, and rheumatoid arthritis with vasculitis. 387 29

Three different experimental models of autoimmune diseases were induced in naive mice after idiotypic immunization. 1) systemic lupus erythematosus (SLE) after injection of anti-DNA antibodies carrying the pathogenic Id-16/6; 2) anti-phospholipid syndrome (APLS) after immunization with anti-cardiolipin antibodies (having the pathogenic H-3 and MIV-7 Ids); and 3) Wegener's granulomatosis (WG) induced with anti-neutrophile cytoplasmic antibodies (ANCA). In all three experiments the mice developed the respective anti-Id antibodies (Ab2), and, after a follow-up period of 4-8 months anti-anti-Id (Ab3) were generated by the immunized mice. The latter antibodies (Ab3) had the binding characteristics of the respective autoantibodies (Ab1) used in the first immunization. The appearance of auto-antibodies in the sera of the mice was associated with emergence of all the typical clinical and laboratory findings seen in patients with SLE, APLS, and WG, respectively. We suggest that in some autoimmune diseases, especially in those in which the presumed autoantigen is not immunogenic (e.g., DNA, cardiolipin), the disease may follow a common infection: The antibodies against the infecting agent may carry a pathogenic idiotype of a specific autoantibody. In a subject prone to autoimmunity (genetic, hormonal, immunologic factors), the pathogenic idiotype will progress in dysregulating the immune system to evolve into a clinical overt autoimmune disease.
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PMID:Idiotypic induction of autoimmunity: a new aspect of the idiotypic network. 800 42