Disease relevance of Lupus

• Efficacy of mycophenolate mofetil in patients with diffuse proliferative lupus nephritis [1].
• METHODS: In a study of 119 women with a history of venous thromboembolism during pregnancy and the puerperium and 233 age-matched normal women, we measured the activity of antithrombin, protein C, protein S, and lupus anticoagulant [2].
• A SNP in the gene PTPN22 is associated with type 1 diabetes, rheumatoid arthritis, lupus, Graves thyroiditis, Addison disease and other autoimmune disorders [3].
• PI3Kgamma inhibition blocks glomerulonephritis and extends lifespan in a mouse model of systemic lupus [4].
• These data support the hypothesis that some humoral autoimmunity in human lupus arises through molecular mimicry between EBNA-1 and lupus autoantigens and provide further evidence to suspect an etiologic role for Epstein-Barr virus in SLE [5].

Psychiatry related information on Lupus

• Such antibodies were infrequent in the long-term therapy group, most of whose members exhibited anti-single-strand DNA and were symptomatic with overt procainamide-induced lupus [6].
• Electroconvulsive therapy and cyclophosphamide in combination for severe neuropsychiatric lupus with catatonia [7].
• Affinity absorption experiments with sera from individual lupus patients showed that up to 41% of the anti-single-stranded DNA antibodies were Id positive [8].
• Demographic, clinical, socioeconomic, and psychosocial factors and disease outcomes [Systemic Lupus Activity Measure (SLAM), Systemic Lupus International Collaborating Clinics/American College of Rheumatology (SLICC/ACR), SF-36] were measured [9].
• Depressive symptoms in patients with systemic lupus erythematosus: association with central nervous system lupus and Sjögren's syndrome [10].

High impact information on Lupus

• BACKGROUND: The combination of cyclophosphamide and prednisolone is effective for the treatment of severe lupus nephritis but has serious adverse effects [11].
• Efficacy of mycophenolate mofetil in patients with diffuse proliferative lupus nephritis. Hong Kong-Guangzhou Nephrology Study Group [11].
• Diltiazem and subacute cutaneous lupus erythematosus-like lesions [12].
• To test the hypothesis that the vasoconstrictor thromboxane A2 may affect renal hemodynamics in lupus nephritis, we examined the short-term effects of a selective thromboxane-receptor antagonist, BM 13,177, and of low-dose aspirin [13].
• Association of antibody to histone complex H2A-H2B with symptomatic procainamide-induced lupus [14].

Chemical compound and disease context of Lupus

• No objective marker for symptomatic procainamide-induced lupus has been described [14].
• This activity was absent in patients not treated with procainamide and in patients with lupus induced by hydralazine or quinidine [14].
• Other manifestations of lupus improved markedly in most cases, despite a reduction in the mean daily dose of prednisone, from 45 mg at entry to 17 mg at follow-up (P less than 0.01) [15].
• Hydrazine and lupus [16].
• Suppression of murine lupus erythematosus by dactinomycin [17].

Biological context of Lupus

• We conclude that acetylator phenotype influences the rate at which procainamide induces antinuclear antibodies and probably the lupus syndrome [18].
• Here we present evidence that the tumour necrosis factor (TNF-alpha) gene, which is located within the H-2 complex (the murine major histocompatibility complex), could be involved in the pathogenesis of lupus nephritis in F1 mice [19].
• (B6.NZMc1[Sle1] x NZW)F1 hybrids develop severe humoral autoimmunity and fatal lupus nephritis, indicating that suppression of Sle1 from NZW is recessive [20].
• Fourteen male patients examined for a prolonged partial thromboplastin time were found to have the lupus anticoagulant [21].
• Influence of thymic genotype on the systemic lupus erythematosus-like disease and T cell proliferation of MRL/Mp-lpr/lpr mice [22].

Anatomical context of Lupus

• Inhibition of protein C activation by endothelial cells in the presence of lupus anticoagulant [23].
• Human lupus T cells resist inactivation and escape death by upregulating COX-2 [24].
• Transgenic animals overexpressing zTNF4 in lymphoid cells develop symptoms characteristic of systemic lupus erythaematosus (SLE) and expand a rare population of splenic B-Ia lymphocytes [25].
• The lpr mice develop lymphadenopathy and suffer from a systemic lupus erythematosus-like autoimmune disease, indicating an important role for Fas antigen in the negative selection of autoreactive T cells in the thymus [26].
• Raji cells, a human B lymphoblastoid cell line of Burkitt lymphoma origin, formed lupus inclusions when grown in a medium conditioned by the growth of Raji cells whose DNA thymidine residues had been unifilarly (single-strandedly) substituted with bromodeoxyuridine [27].

Gene context of Lupus

• Sle1 and Sle3 are NZW-derived loci that mediate lupus nephritis on a C57BL/6 background [20].
• These data demonstrate a functionally significant phenotype for the NZM2410 Cr2 allele and strongly support its role as a lupus susceptibility gene [28].
• Cr2, a candidate gene in the murine Sle1c lupus susceptibility locus, encodes a dysfunctional protein [28].
• These inhibitors of TLR signaling thus represent novel therapeutic agents with potential for the treatment of lupus [29].
• Roles of interferon-gamma and interleukin-4 in murine lupus [30].

Analytical, diagnostic and therapeutic context of Lupus

• Retrospective studies of patients in whom procainamide lupus had developed revealed that the duration of therapy required for induction in 14 slow and seven rapid acetylators was 12 +/- 5 and 48 +/- 22 months respectively (P less than 0.002) [18].
• In view of earlier reports that implicated IgM in poor pregnancy outcome, particularly in association with systemic lupus erythematosus, it is suggested that all patients with circulating lupus anticoagulant syndrome be evaluated for an IgM gammopathy [31].
• In contrast, none of the lupus sera reacted with synthetic peptides in ELISA [32].
• The remaining five lupus sera were able to immunoprecipitate translation products as well as Western blot recombinant fusion proteins [32].
• Vaccination with minigenes encoding V(H)-derived major histocompatibility complex class I-binding epitopes activates cytotoxic T cells that ablate autoantibody-producing B cells and inhibit lupus [33].

References