? Monoclonal Antibody and Reagent Core This Program Project addresses the impact of antibodies cross-reactive to DNA and the N-methyl D-aspartate receptor (NMDAR), DNRAbs, on adult and fetal brain. The premise of the program is that DNRAbs induce a chronic inflammatory state in the adult brain and permanent cognitive impairment in offspring exposed to these antibodies in vitro Projects 1 and 3 both utilize a panel of monoclonal DNRAbs. These need to be produced in large quantity. The Monoclonal Antibody and Reagent Core will produce both human and murine antibodies and will test these for preservation of antigen binding. The Core will produce antibody that is validated for binding to DNA, DWEYS and the extracellular domains of GluN2A/B. The Core will generate GluN2A/B extracellular domains for use in ELISAs to confirm antibody specificity. Projects 2 and 3 requires that serum be tested for DNRAb titer. The Core will provide quality control for these assays also. Project 3 will need large amounts of decoy antigen of high purity to be produced. This facility will be cost-effective and will maintain quality control for all 3 projects in the Program. This represents an efficient approach to the generation of reagents to be used by multiple investigators and one that maximizes the production of high quality reagents. Antibodies represent a highly versatile tool in medical research. They are used in diagnostics, in basic and clinical research and in developing new therapies. The DNRAbs created in our laboratory are utilized in all of the above areas not only in our studies but in many laboratories within the United States and abroad.
? Monoclonal Antibody and Reagent Core This Core will provide monoclonal antibodies and assessments of antibody titer for the studies in the Program Project and for laboratories world-wide that are interested in initiating basic or clinical studies of neuropsychiatric lupus. The Core will also produce decoy antigens once a lead candidate is identified. The studies enabled by these antibodies will hasten clinical strategies for neuroprotection in patients with lupus.
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|Kim, Sook Young; Son, Myoungsun; Lee, Sang Eun et al. (2018) High-Mobility Group Box 1-Induced Complement Activation Causes Sterile Inflammation. Front Immunol 9:705|
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|Mader, Simone; Brimberg, Lior; Soltys, John N et al. (2018) Mutations of Recombinant Aquaporin-4 Antibody in the Fc Domain Can Impair Complement-Dependent Cellular Cytotoxicity and Transplacental Transport. Front Immunol 9:1599|
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|Honig, Gerard; Mader, Simone; Chen, Huiyi et al. (2016) Blood-Brain Barrier Deterioration and Hippocampal Gene Expression in Polymicrobial Sepsis: An Evaluation of Endothelial MyD88 and the Vagus Nerve. PLoS One 11:e0144215|
|Malkiel, Susan; Jeganathan, Venkatesh; Wolfson, Stacey et al. (2016) Checkpoints for Autoreactive B Cells in the Peripheral Blood of Lupus Patients Assessed by Flow Cytometry. Arthritis Rheumatol 68:2210-20|
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