BIMS Affiliated Research Faculty

All Research Faculty

 
Ronald  P.  Taylor
Degree(s): PhD
Graduate School: Princeton University
Primary Appointment: Professor, Biochemistry and Molecular Genetics
Research Interests:
Clearance of Pathogens: The role of complement in Immunotherapy: New approaches to vaccine generation
Email Address: rpt@virginia.edu

Biomedical Sciences Graduate Program(s)
  • Biomedical Sciences Graduate Programs

  • Research Description

    The long-term goal of our research is to provide an experimental foundation for the general treatment of infectious diseases through use of heteropolymer (HP)-sensitized human erythrocytes (RBCs). We have prepared bi-specific cross-linked monoclonal antibodies (HPs) with specificity for both selected targeted pathogens and the human erythrocyte C3b complement receptor (CR1). These HPs facilitate rapid and quantitative in vitro binding of targeted pathogens to CR1 on human and other primate RBCs. The use of HPs allows us to bypass the complement opsonization requirement for binding of immune complex substrates to CR1. Virtually any potential pathogen can be selectively bound to RBCs by this procedure. The HPs facilitate in vivo binding of innocuous prototype pathogens to primate RBCs, and these RBC-bound substrates and HP are rapidly cleared from the circulation without any lysis or sequestration of the RBCs. This result is a manifestation of one of the body's natural defenses, the RBC-based immune complex clearance mechanism. This mechanism allows for the safe and rapid neutralization and clearance of complement-opsonized pathogens bound to CR1 on human and non-human primate RBCs. We are now investigating whether virulent pathogens will be bound in vivo to RBCs via appropriately constructed HPs, and then rapidly and safely cleared from the circulation. Selected particulate pathogens include several bacteria and viruses. We are also developing general approaches for the treatment of cancer based on the interaction of cancer cells with the complement sysstem. In the presence of serum and normal human IgM and/or specific monoclonal antibodies, large amounts of the complement activation product, C3bi, covalently bind to the cancer cells. We are using monoclonal antibodies specific for cell-associated C3bi to facilitate tumor cell targeting and killing.


    Selected Publications
  • Daubeuf, S, Lindorfer, MA, Taylor, RP, Joly, E and Hudrisier, D. The direction of plasma membrane exchange between lymphocytes and accessory cells by trogocytosis is influenced by the nature of the accessory cell. J. Immunol., 184: 1897-1908, 2010 PMID: 20089699.
  • Taylor, RP and Lindorfer, MA. Antigenic Modulation and Rituximab Resistance. Seminars in Hematology, 47:124-132, 2010. PMID: 20350659.
  • Pawluczkowycz, AW, Beurskens, FJ, Beum, PV, Lindorfer, MA, van de Winkel, JGJ, Parren, PWHL, Taylor, RP Binding of Submaximal C1q Promotes Complement Dependent Cytotoxicity (CDC) of B cells Opsonized with anti-CD20 mAbs Ofatumumab (OFA) or Rituximab (RTX). Considerably Higher Levels of CDC are Induced by OFA Than by RTX. J. Immunol., 183: 749-758, 2009 PMID: 19535640.
  • Beum, PV, Lindorfer, MA, Taylor, RP Within Peripheral Blood Mononuclear Cells, Antibody-Dependent Cellular Cytotoxicity of Rituximab-opsonized Daudi cells is Promoted by Natural Killer Cells and Inhibited by Monocytes Due to Shaving. J. Immunol., 181: 2916-2924, 2008 PMID: 18684983.
  • PubMed Listings for this Faculty Member

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    Contact Information
      Office Address: PO Box 800733 Jordan Hall, 6023, 
      Office Phone: +1 434-924-2664
      Fax Phone: +1 434-924-5069

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