DNA released from dying host cells mediates aluminum adjuvant activity

摘要: Aluminum-based adjuvants (aluminum salts or alum) are widely used in human vaccination, although their mechanisms of action poorly understood. Here we report that, mice, alum causes cell death and the subsequent release host DNA, which acts as a potent endogenous immunostimulatory signal mediating adjuvant activity. Furthermore, propose that DNA signaling differentially regulates IgE IgG1 production after alum-adjuvanted immunization. We suggest on one hand, induces primary B responses, including production, through interferon response factor 3 (Irf3)-independent mechanisms. On other also stimulates 'canonical' T helper type 2 (T H 2) associated with isotype switching peripheral effector Irf3-dependent The finding released from dying cells damage-associated molecular pattern mediates activity may increase our understanding current vaccines help design new adjuvants.