R
Ronald P. Taylor
Researcher at University of Virginia
Publications - 222
Citations - 8729
Ronald P. Taylor is an academic researcher from University of Virginia. The author has contributed to research in topics: Antibody & Complement system. The author has an hindex of 47, co-authored 217 publications receiving 8075 citations. Previous affiliations of Ronald P. Taylor include Carter Center.
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Journal ArticleDOI
Complement is activated by IgG hexamers assembled at the cell surface.
Christoph A. Diebolder,Christoph A. Diebolder,Frank J. Beurskens,Rob N. de Jong,Roman I. Koning,Kristin Strumane,Margaret A. Lindorfer,Marleen Voorhorst,Deniz Ugurlar,Sara Rosati,Albert J. R. Heck,Jan G. J. van de Winkel,Ian A. Wilson,Abraham J. Koster,Ronald P. Taylor,Erica Ollmann Saphire,Dennis R. Burton,Dennis R. Burton,Janine Schuurman,Piet Gros,Paul W. H. I. Parren +20 more
TL;DR: This work found that specific noncovalent interactions between Fc segments of immunoglobulin G (IgG) antibodies resulted in the formation of ordered antibody hexamers after antigen binding on cells, thereby triggering the complement cascade.
Journal ArticleDOI
Mechanisms of killing by anti-CD20 monoclonal antibodies.
TL;DR: How monoclonal antibodies (mAb) have driven research in the immunotherapy field over the last decade are discussed, their likely modes of action and their limitations in terms of effector exhaustion are explored, and ways in which they might be enhanced and further exploited in the future are explored.
Journal ArticleDOI
Rituximab Infusion Promotes Rapid Complement Depletion and Acute CD20 Loss in Chronic Lymphocytic Leukemia
Adam D. Kennedy,Paul V. Beum,Michael D. Solga,David J. DiLillo,Margaret A. Lindorfer,Charles E. Hess,John J. Densmore,Michael E. Williams,Ronald P. Taylor +8 more
TL;DR: In vitro studies indicate that at high cell densities, binding of rituximab to human CD20+ cells leads to loss of complement activity and consumption of component C2, and western blots provide additional evidence for this escape mechanism that appears to occur as a consequence of CD20 loss.
Journal Article
Disease-associated loss of erythrocyte complement receptors (CR1, C3b receptors) in patients with systemic lupus erythematosus and other diseases involving autoantibodies and/or complement activation.
G D Ross,William J. Yount,Mark Walport,J B Winfield,Charles J. Parker,C R Fuller,Ronald P. Taylor,B L Myones,Peter J. Lachmann +8 more
TL;DR: The number of CR1 per E was quantitated with 125I-monoclonal anti-CR1 and was found to vary inversely with disease activity in patients with SLE who were followed serially for as long as 14 mo, andKinetic experiments indicated that C3b was fixed to E during the process of immune complex binding and release from E CR1, and that this fixed C3B was subsequently degraded rapidly to fixed iC3b and more slowly to fixed C
Journal ArticleDOI
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.
Andrew W. Pawluczkowycz,Frank J. Beurskens,Paul V. Beum,Margaret A. Lindorfer,Jan G. J. van de Winkel,Paul W. H. I. Parren,Ronald P. Taylor +6 more
TL;DR: The role of C1q in the dynamics of complement activation and CDC of B cell lines and primary cells from patients with chronic lymphocytic leukemia, reacted with OFA or RTX is examined.