J
Jeffrey V. Ravetch
Researcher at Rockefeller University
Publications - 310
Citations - 59480
Jeffrey V. Ravetch is an academic researcher from Rockefeller University. The author has contributed to research in topics: Antibody & Receptor. The author has an hindex of 110, co-authored 296 publications receiving 54829 citations. Previous affiliations of Jeffrey V. Ravetch include Bristol-Myers Squibb & Kettering University.
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Journal ArticleDOI
Antibodies, Fc receptors and cancer
TL;DR: Novel insights into antibody FcR interactions might be useful to produce the next generation of improved immunotherapeutic molecules.
Journal ArticleDOI
Modulating IgG effector function by Fc glycan engineering.
Tiezheng Li,David J. DiLillo,Stylianos Bournazos,John P. Giddens,Jeffrey V. Ravetch,Lai-Xi Wang +5 more
TL;DR: It is found that core fucosylation exerted a significant adverse effect on FcγRIIIA binding, in vitro ADCC, and in vivo IgG-mediated cellular depletion, regardless of sialylation status.
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IgG antibodies to dengue enhanced for FcγRIIIA binding determine disease severity
Taia T. Wang,Taia T. Wang,Jaturong Sewatanon,Jaturong Sewatanon,Matthew J. Memoli,Jens Wrammert,Stylianos Bournazos,Siddhartha Kumar Bhaumik,Benjamin A. Pinsky,Kulkanya Chokephaibulkit,Nattawat Onlamoon,Kovit Pattanapanyasat,Jeffery K. Taubenberger,Rafi Ahmed,Jeffrey V. Ravetch +14 more
TL;DR: It is discovered that DHF/DSS patients respond to infection by producing IgGs with enhanced affinity for the activating Fc receptor FcγRIIIA due to afucosylated Fc glycans and IgG1 subclass, which is implicated in severe dengue disease during secondary infections.
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Restoration of Tolerance in Lupus by Targeted Inhibitory Receptor Expression
TL;DR: It is demonstrated that the partial restoration of inhibitory Fc receptor (FcgRIIB) levels on B cells in lupus-prone mouse strains is sufficient to restore tolerance and prevent autoimmunity.
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The inhibitory Fcgamma receptor modulates autoimmunity by limiting the accumulation of immunoglobulin G+ anti-DNA plasma cells.
TL;DR: FcγRIIB provides a distal peripheral checkpoint to limit the accumulation of autoreactive plasma cells, thereby maintaining tolerance, and is investigated using gene-targeted immunoglobulin variable heavy-chain (VH) alleles 3H9 or 56R, which encode DNA-specific heavy chains.