Development of autoantibodies before the clinical onset of systemic lupus erythematosus.

By M. Arbuckle, M. McClain, M. Rubertone, R. Scofield, G. Dennis, J. James, J. Harley. New England Journal of Medicine, 2003

2,480 citations recorded by the source corpus.

Subfields: Hepatology, Pathology and Forensic Medicine, Rheumatology

View Paper: https://www.semanticscholar.org/paper/f97a0382a91911170f4a970e01a26fd3dd73f4d4

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In Pathology and Forensic Medicine

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Citations in the corpus

Personalized Immunomonitoring Uncovers Molecular Networks That Stratify Lupus Patients (2016, neutral): “…progression, whereby an initial increase in IFN response and differentiation of B cells into short-lived plasmablasts, which may occur before clinical onset (Arbuckle et al., 2003), is fol- lowed by kidney disease and full-blown systemic inflammation fueled by myeloid cells, including neutrophils.”
Analysis of families in the multiple autoimmune disease genetics consortium (MADGC) collection: the PTPN22 620W allele associates with multiple autoimmune phenotypes. (2005, neutral): “Indeed , SLE, RA, T1D, and Hashimoto thyroiditis are all characterized by the frequent development of autoantibodies , often before the onset of clinical disease (Arbuckle et al. 2003; Strieder et al. 2003; Hoppu et al. 2004; Nielen et al. 2004).”
'ASIA' - autoimmune/inflammatory syndrome induced by adjuvants. (2011, background): “autoantibodies) appears years before a full blown autoimmune disease is diagnosed [25].”
Genetic association of the R620W polymorphism of protein tyrosine phosphatase PTPN22 with human SLE. (2004, background): “All three of the human autoimmune diseases shown to date to be associated with PTPN22 R620W are characterized by the production of autoantibodies (anti-GAD Abs in T1D, anti-citrulline Abs and rheumatoid factor in RA, and a vast array of autoantibodies in SLE), and the appearance of these antibodies ”
Competence and competition: the challenge of becoming a long-lived plasma cell (2006, background): “Similarly, the presence of charac-teristic serum autoantibodies before the onset of disease has been observed in patients with type 1 diabetes, SLE or coeliac diseas”
Type I interferon in systemic lupus erythematosus and other autoimmune diseases. (2006, background): “Ro, La, and phospholipid antibodies appear first, followed by dsDNA antibodies and then Sm and nuclear ribonucleoprotein antibodies (Arbuckle et al., 2003).”
Human lupus autoantibody-DNA complexes activate DCs through cooperation of CD32 and TLR9. (2005, background): “These autoantibodies are thought to contribute directly to the pathogenesis of SLE, as they precede the development of clinical disease in most patients, and levels of anti-DNA antibodies correlate with disease activity (4, 5).”