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Van Bruggen, M.C., Walgreen, B., Rijke, T.P., Corsius, M.J., Assmann, K.J., Smeenk, R.J., et al. (1996) Heparin and Heparinoids Prevent the Binding of Immune Complexes Containing Nucleosomal Antigens to the GBM and Delay Nephritis in MRL/LPR Mice. Kidney International, 50, 1555-1564.
https://doi.org/10.1038/ki.1996.471

has been cited by the following article:

• TITLE: In Lupus Erythematosus the Deposition of Immune Complexes in Tissues Is Mediated via Nuclear Histones Released by Neutrophils Nets but the Main Damage to Hosts Tissues Is Caused by the Plethora of Toxic Pro Inflammatory Agents Released by Activated Neutrophils—A Working Hypothesis

  AUTHORS: Isaac Ginsburg

  KEYWORDS: Auto Immune Destructive Disorder, Lupus Erythematosus

  JOURNAL NAME: Open Journal of Rheumatology and Autoimmune Diseases, Vol.10 No.2, May 29, 2020

  ABSTRACT: The present study offers a novel approach that may explain the mechanisms of pathogenicity of the auto immune destructive disorder, Lupus Erythematosus. It is proposed that deposition of immune complexes and complement components in tissue is mediated by highly cationic histones released from neutrophils nets the phenomenon of netosis. Histones act a potent opsonic factor similar to antibodies which interact by strong electrostatic forces with negatively-charged domains in immune complexes and complements facilitating their deposition and also their internalization by hosts’ cells. However, the main cause of cell and tissue damage in Lupus is inflicted by the plethora of toxic pro inflammatory agonists released by neutrophils and by macrophages recruited to inflamed tissues by cytokines. The melioration of tissue damage may be initiated by highly anionic heparins, which neutralizes histones’ action if also combined with steroids, colchicin and methtorxate as well as by other agents which retard leukocytes migration and functions.