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Systemic Lupus Erythematosus
Published in Jason Liebowitz, Philip Seo, David Hellmann, Michael Zeide, Clinical Innovation in Rheumatology, 2023
Vaneet K. Sandhu, Neha V. Chiruvolu, Daniel J. Wallace
Early in the history of SLE research, investigators relied on the lupus erythematosus (LE) cell phenomenon and assessed the presence of LE cells (the pathophysiology of which will be discussed later) in peripheral blood or autopsy pathology as a tool for SLE diagnosis. Researchers soon realized that LE cells alone were not reliable markers as they are not always present in SLE. Instead, they sought to group clinical, laboratory, and pathological manifestations of SLE to create criteria to aid in diagnosis. It wasn’t until 1971 that a strict set of criteria for epidemiological and research use would be established to assist in classifying individuals with SLE.2, 3
The Musculoskeletal System and Its Disorders
Published in Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss, Understanding Medical Terms, 2020
Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss
Systemic lupus erythematosus is diagnosed by presentation of a number of clinical symptoms, most commonly arthralgia (arth = joint, algia = pain) and arthritis. Laboratory tests show abnormal ANA titer, positive LE cell test. Several different drugs are utilized in the treatment of systemic lupus erythematosus. Aspirin and the NSAIDs are used to manage arthralgias or synovitis (inflammation of the synovium), pleurisy, headache, and low-grade fever. The antimalarial agent hydroxychloroquine is effective in treating arthralgias, arthritis, and skin disease. Corticosteroids are used to control the inflammatory response. Connective tissue disorders are treated by rest and exercise, physical and occupational therapy, heat, supportive or rehabilitative devices, education, nutrition, and orthopedic surgery.
Definition, Classification, Activity and Damage Indices in Systemic Lupus Erythematosus
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Jennifer M. Grossman, Kenneth C. Kalunian
The resulting revised criteria consist of 11 items, compared with 14 in the preliminary criteria; 5 of the criteria are composites of one or more abnormalities. As in the preliminary data, patients must fulfill 4 or more criteria; no single criterion is absolutely essential. These criteria are the same as the 1997 revised criteria shown in Table 1, with the exception of criterion 10, which according to the revised 1982 criteria read: immunologic disorder (a) positive LE-cell preparation; OR (b) anti-double-stranded DNA; OR (c) anti-Sm; (d) BFP (false-positive serologic test for syphilis positive for at least 6 months with negative TPI or FTA).
The impact of assay recovery on the apparent permeability, a function of lysosomal trapping
Published in Xenobiotica, 2020
Dallas Bednarczyk, Menaka V Sanghvi
MDCK-LE cells are a low efflux (LE) cell line developed internally at Novartis (Dickson et al., 2019). MDCK-LE cells were cultured at 37 °C under a 5% CO2 atmosphere, at 95% relative humidity in DMEM containing 10% heat inactivated fetal bovine serum, penicillin-streptomycin (100 μg/mL), and 2 mM Ala-Gln. Cells were passaged weekly into an Omnitray (Nunc, Thermo Fisher Scientific, Rochester, NY) at a density of approximately 500,000 cells for continuous culture. For assay purposes, cells were seeded at a density of approximately 75,000 cells/well of a 96-well solid support plate (Greiner Bio-One North America Inc., Monroe, NC) or 37,500 cells/well of a 96-well Transwell plate (Corning Life Sciences, Acton, MA) and cultured in the media noted above for a period of five days.
Active NET formation in Libman–Sacks endocarditis without antiphospholipid antibodies: A dramatic onset of systemic lupus erythematosus
Published in Autoimmunity, 2018
Daniel Appelgren, Charlotte Dahle, Jasmin Knopf, Rostyslav Bilyy, Volodymyr Vovk, Pia C. Sundgren, Anders A. Bengtsson, Jonas Wetterö, Luis E. Muñoz, Martin Herrmann, Anders Höög, Christopher Sjöwall
Nowadays the role of neutrophils in the etiopathogenesis of systemic lupus erythematosus (SLE) attracts highest interest [1,2]. However, with the LE cell test as a key exception, granulocytes have historically been rather neglected in the context of SLE [3,4]. One reason of this paradigm shift is that low-density granulocytes (LDGs), a subset of neutrophils which is increased in SLE, show the capacity to produce type I interferons (IFN) and spontaneously form neutrophil extracellular traps (NETs) [5,6]. The latter consist of decondensed chromatin decorated with neutrophil-derived proteases and antimicrobial peptides that may trap and kill pathogens [7]. Furthermore, “classical” lupus autoantigens, such as histones and double-stranded (ds) DNA have been identified as constituents of NETs and their corresponding autoantibodies may potentially protect the NETs from degradation [8]. In MRL/lpr mice, inhibition of NET release containing mitochondrial DNA ameliorates lupus-like autoimmune disease by down-regulating the type I IFN response [9].