Jeffrey V. Ravetch

TL;DR: These results suggest a two-step model for IVIG protection in which CSF-1-dependent macrophages act as innate "sensors" for the Fc fragment of IVIG, leading to the induction of Fc gamma RIIB on CSF -1-independent "effector" Macrophages thereby raising the threshold required for Fc Gamma RIII activation and preventing autoantibody-triggered inflammation.

TL;DR: The structural heterogeneity of the human low affinity receptor for IgG, FcRII(CD32), has been elucidated through the isolation, characterization, and expression of cDNA clones derived from myeloid and lymphoid RNA that predict amino acid sequences consistent with integral membrane glycoproteins with single membrane spanning domains.

TL;DR: Sialylated IgG Fcs initiate an anti-inflammatory cascade through the lectin receptor SIGN-R1 or DC-SIGN, which leads to upregulated surface expression of the inhibitory FcR, FcγRIIb, on inflammatory cells, thereby attenuating autoantibody-initiated inflammation.

TL;DR: It is revealed that distinct Fcγ receptor (FcγRs) dependency and mechanisms account for the in vivo activity of anti- PD-1 versus anti-PD-L1 Abs, which show augmented anti-tumor activity when activating F cγR binding is introduced into the molecules.

TL;DR: Lu et al. as mentioned in this paper showed that neutralizing antibodies may be a promising therapy for HIV-1 because of their potential to reduce the viral reservoir, and demonstrated that therapeutic antibody treatment enhanced infected individuals' humoral response against the virus.