My unique single-domain antibodies我唯一的单域抗体.pptVIP

At least three mechanisms for immunotherapy of AD have been proposed. Two mechanisms, microglial activation (8, 9) and catalytic dissolution (10), require that the antibody enter the central nervous system; the other mechanism, sometimes called the peripheral sink hypothesis, does not. In the microglial activation mechanism (8), antibodies bind to amyloid plaques, triggering microglia via their Fc receptors. As evidence for this mechanism, A(1–42) immunization elicits synthesis of anti-A antibodies and causes A-reactive microglial cells to appear around plaques (8). In catalytic dissolution, antibodies are hypothesized to act as chaperones, catalyzing the structural * At least three mechanisms for immunotherapy of AD have been proposed. Two mechanisms, microglial activation (8, 9) and catalytic dissolution (10), require that the antibody enter the central nervous system; the other mechanism, sometimes called the peripheral sink hypothesis, does not. In the microglial activation mechanism (8), antibodies bind to amyloid plaques, triggering microglia via their Fc receptors. As evidence for this mechanism, A(1–42) immunization elicits synthesis of anti-A antibodies and causes A-reactive microglial cells to appear around plaques (8). In catalytic dissolution, antibodies are hypothesized to act as chaperones, catalyzing the structural the peripheral sink hypothesis: Consistent with this mechanism, the efficacy of a given mAb depends on the A sequence element it binds; thus, the mAb 6C6, which recognizes the A N terminus, is three times more effective in disaggregating A fibrils than the mAb 1C2, which binds to the central residues of A (10). In the peripheral sink hypothesis (3), antibodies bind to A in the bloodstream, shifting the distribution of A between the brain and the peripheral circulatory system and thereby leading to a net efflux of A from the central nervous system to plasma, where it is degraded. Thus, DeMattos et al. (3) observed a 1,000-fold increase in