Disease relevance of Lupus Erythematosus, Systemic

• B cell hyperactivity, hypergammaglobulinemia, and autoantibody expression, the hallmarks of systemic lupus erythematosus, might be associated with structural abnormalities within the Ig heavy chain variable region (Igh-V) gene complex [1].
• By induction of a graft-vs.-host reaction (GVHR) in nonirradiated H-2-different F1 mice, one can induce stimulatory pathological symptoms, such as lymphadenopathy and hypergammaglobulinemia, combined with the production of autoantibodies characteristic of systemic lupus erythematosus (SLE) [2].
• Anti-C1q autoantibodies are present in sera of patients with several autoimmune diseases, including systemic lupus erythematosus (SLE) [3].
• We compared the clinical development (autoantibody production and glomerulonephritis) of systemic lupus erythematosus (SLE) in these three F1 hybrids in the presence or absence of the mutant gene, Yaa (Y chromosome-linked autoimmune acceleration), which normally accelerates the progression of murine SLE [4].
• This approach provides unique molecular signatures for rheumatoid arthritis, systemic lupus erythematosus, and graft versus host disease, and can also be applied to defining the molecular phenotype of a variety of other normal and pathological processes [5].

High impact information on Lupus Erythematosus, Systemic

• In the population (and in the autoimmune mouse strain MRL/lpr) there is a great variety of such antinuclear antibodies, but individuals with systemic lupus erythematosus or single MRL mice express a subset only of the antinuclear specificities found in the population [6].
• The major murine systemic lupus erythematosus (SLE) susceptibility locus, Sle1, corresponds to three loci independently affecting loss of tolerance to chromatin in the NZM2410 mouse [7].
• Renal papillary necrosis occurred after fenoprofen calcium administration in a patient with systemic lupus erythematosus and urinary tract infection [8].
• Dendritic cell (DC) activation by nucleic acid-containing immunoglobulin (Ig)G complexes has been implicated in systemic lupus erythematosus (SLE) pathogenesis [9].
• Genetic modifiers of systemic lupus erythematosus in FcgammaRIIB(-/-) mice [10].

Chemical compound and disease context of Lupus Erythematosus, Systemic

• Selective suppression of retroviral gp70-anti-gp70 immune complex formation by prostaglandin E1 in murine systemic lupus erythematosus [11].
• Estrogen can modulate autoimmunity in certain models of systemic lupus erythematosus [12].
• Short term administration of costimulatory blockade and cyclophosphamide induces remission of systemic lupus erythematosus nephritis in NZB/W F1 mice by a mechanism downstream of renal immune complex deposition [13].
• Heparin was found to inhibit the DNA binding of antibodies eluted from kidneys of both humans and MRL-lpr/lpr mice with systemic lupus erythematosus [14].
• The role of complement C3 in mediating systemic lupus erythematosus (SLE) was examined using a double-knockout C3(null)C4(null) Fas (CD95)-deficient mouse model [15].

Biological context of Lupus Erythematosus, Systemic

• The present study indicates that the cryoglobulin activity associated with the gamma 3 isotype is critically involved in the pathogenicity of 6-19 anti-IgG2a rheumatoid factor monoclonal antibody and highlights the pathogenic relevance of autoantibodies of the IgG3 subclass in murine systemic lupus erythematosus [16].
• An Ig mu-heavy chain transgene inhibits systemic lupus erythematosus immunopathology in autoimmune (NZB x NZW)F1 mice [17].
• BWF1 mice, a murine model for systemic lupus erythematosus (SLE), implanted with Silastic tubes containing DES after orchidectomy developed murine lupus characterized by immunoglobulin G (IgG) anti-DNA antibody production and IgG deposition in the glomeruli in the kidney as well as those implanted with 17beta-estradiol (E2) [18].
• BACKGROUND: MRL/MpJ-Tnfrsf6lpr(MRL/lpr) mice, a murine model of systemic lupus erythematosus (SLE), have defective expression of Fas, substantially reducing signaling for apoptosis via this mechanism [19].
• In chronic pathologies like autoimmune hemolytic anemia in the NZB mouse strain or systemic lupus erythematosus (SLE) in the BXSB mouse strain, TWEAK mRNA was shown to be reduced concomitantly to the development of chronic autoimmune diseases [20].

Anatomical context of Lupus Erythematosus, Systemic

• Absolute numbers of B (IgG-, IgM-, and IgA-staining) and T lymphocytes (sheep erythrocyte rosette-forming cells) were determined in patients with systemic lupus erythematosus and other connective tissue diseases in cyclophosphamide-treated and noncyclophosphamide-treated patients and in control subjects [21].
• Macrophages from nonobese diabetic (NOD) mice, which spontaneously develop type I diabetes, share a defect in elicited cytokine production with macrophages from multiple diverse strains of systemic lupus erythematosus (SLE)-prone mice [22].
• The quantity of P-gp on SLE lymphocytes correlated with the disease activity in each patient, as estimated by the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) [23].
• Our results support the concept that the high prevalence of coronary artery disease in systemic lupus erythematosus is due in part to a reduction of HDL cholesterol levels resulting from the autoimmune disease [24].
• The brains of pathogen-free autoimmune MRL/lpr, NZBWF1 and NZB mice were examined for central nervous system (CNS) inflammation in premoribund 8-week-old animals and at ages when active systemic lupus erythematosus (SLE) was present [25].

Gene context of Lupus Erythematosus, Systemic

• Epistatic suppression of systemic lupus erythematosus: fine mapping of Sles1 to less than 1 mb [26].
• Susceptibility to systemic lupus erythematosus in the NZM2410 murine model maps to Sle1, Sle2, Sle3, and the H2 loci [27].
• Mutation in genes encoding Fas (Ipr) and the Fas ligand (gld) contribute to the development of an autoimmune syndrome similar to systemic lupus erythematosus in mice [28].
• Defects of early complement components (C1, C4 and C2) are associated with the development of systemic lupus erythematosus (SLE) [29].
• As has been reported previously, models of chronic graft-versus-host (GvH) and systemic lupus erythematosus (SLE)-like diseases are characterized by high IgE and IgG1 immunoglobulin (Ig) levels in the serum [30].

Analytical, diagnostic and therapeutic context of Lupus Erythematosus, Systemic

• We report in this study that MRL/lpr mice, an animal model of systemic lupus erythematosus, have increased splenic expression of Fli-1 protein compared with BALB/c mice [31].
• The authors describe here in detail the age-related histologic changes in pulmonary inflammation, the age-related changes in bronchoalveolar lavage (BAL), and the effect of cyclophosphamide (8 mg/kg) on pulmonary inflammation and bronchoalveolar lavage in MRL/Mp-lpr/lpr mouse, an animal model of systemic lupus erythematosus [32].
• Using the Western blot technique we analyzed the sera of five strains of mice that develop a disease like systemic lupus erythematosus (SLE), along with two normal strains, for their binding specificities against isolated mouse integral brain membrane proteins [33].
• After gene therapy, clinical signs of systemic lupus erythematosus were reduced dramatically: the anti-nuclear antibody titers and urine protein/creatinine ratios were recovered to normal values, and the skin regained its normal histological features [34].
• Mycophenolate mofetil (MMF), an immunosuppressive drug commonly used in organ transplantation, is increasingly being used to treat autoimmune diseases including systemic lupus erythematosus (SLE) [35].

References