Scientists at UMC Utrecht reported two FcγRI‑specific antibodies (C01 and C04) that competitively block high‑affinity IgG binding to CD64 (FcγRI) and suppress autoimmune responses in preclinical models. Structural studies showed C01 binds within FcγRI’s IgG‑binding site; both antibodies displaced immune complexes and blocked binding up to 90% without triggering receptor activation. In humanized mouse models of immune thrombocytopenia, the antibodies significantly reduced IgG‑dependent platelet depletion, demonstrating in vivo efficacy. The antibodies are Fc‑silent and avoid receptor clustering that can provoke cytokine release — a critical safety advantage over prior anti‑FcγRI attempts. Authors suggest these blockers could offer a new therapeutic route for FcγRI‑driven autoimmune diseases including rheumatoid arthritis and lupus. Clarification: FcγRI (CD64) is a high‑affinity IgG receptor on myeloid cells that mediates immune complex‑driven inflammation; blocking it can dampen pathogenic antibody responses.