Is antibody therapy of tumor compromised by infusion-related reactions? A case for inhibiting the activity of cyclooxygenase-2.

摘要: Abstract Evidence suggests that amelioration of childhood immune thrombocytopenic purpura and some other autoimmune states by intravenous normal IgG is due to the following chain events: (1) cross-linking Fcγ-receptors on blood effector cells; (2) release mediators from these cells, often yielding an infusion-related reaction; (3) mediator-induced development a cytokine field characterized mutually stabilizing Th2 polarization CD4 T lymphocytes alternative activation macrophages; (4) selective quiescence macrophages towards targets coated with autoantibody, increased expression macrophage Fcγ-receptor IIB. In this paper it postulated in antibody therapy tumor, undesirable delayed or absent subsidence antibody-coated tumor immunomodulation same type as yields autoimmunity, arising similar events. If postulate correct could usefully be broken at level mediator action, possibly blocking synthesis prostaglandin E 2 which catalyzed enzyme cyclooxygenase-2.