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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Inhibitory Fc receptors modulate in vivo cytotoxicity against tumor targets.
TL;DR: It is demonstrated that Fc-receptor-dependent mechanisms contribute substantially to the action of cytotoxic antibodies against tumors and indicate that an optimal antibody against tumors would bind preferentially to activation Fc receptors and minimally to the inhibitory partner FcγRIIB.
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Fcγ receptors as regulators of immune responses
TL;DR: Recent studies addressing the multifaceted roles of FcRs for IgG (FcγRs) in the immune system are discussed and how this knowledge could be translated into novel therapeutic strategies to treat human autoimmune, infectious or malignant diseases are discussed.
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Dendritic Cells Induce Peripheral T Cell Unresponsiveness under Steady State Conditions in Vivo
Daniel Hawiger,Kayo Inaba,Kayo Inaba,Yair Dorsett,Ming Guo,Karsten Mahnke,Miguel Rivera,Jeffrey V. Ravetch,Ralph M. Steinman,Michel C. Nussenzweig,Michel C. Nussenzweig +10 more
TL;DR: An antigen delivery system targeting these specialized antigen presenting cells in vivo using a monoclonal antibody to a DC-restricted endocytic receptor is devised, which concludes that in the absence of additional stimuli DCs induce transient antigen-specific T cell activation followed by T cell deletion and unresponsiveness.
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IgG Fc Receptors
TL;DR: Fc gamma Rs offer a paradigm for the biological significance of balancing activation and inhibitory signaling in the expanding family of activation/inhibitory receptor pairs found in the immune system.
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Anti-Inflammatory Activity of Immunoglobulin G Resulting from Fc Sialylation
TL;DR: It is shown that IgG acquires anti-inflammatory properties upon Fc sialylation, which is reduced upon the induction of an antigen-specific immune response, and may provide a switch from innate anti- inflammatory activity in the steady state to generating adaptive pro-inflammatory effects upon antigenic challenge.