针对污染导致的近海生态功能退化与生态服务价值下降的现状，以新型持久性有机污染物多溴联苯醚(PBDEs)为胁迫因子，首次在近海环境岗哨生物—紫贻贝(Mytilus edulis)的血细胞中开展PBDEs胁迫-应答的免疫权衡策略与免疫应答机制研究。主要回答两个问题：1、紫贻贝血细胞能够随着环境变化权衡其免疫应答过程，这种应答是可塑的。从免疫功能与能量代价分析入手阐明血细胞响应PBDEs胁迫的免疫权衡策略及其环境可塑性；2、紫贻贝血细胞中的免疫相关基因/关键氧化还原敏感蛋白质决定其对PBDEs的免疫响应。以氧化还原机制为切入点，围绕Nrf2/ARE通路展开研究。构建高可操作性的氧化还原蛋白质组学技术与比较转录组技术相结合的研究方法，高通量且彼此互补地分析参与PBDEs免疫应答关键过程的免疫相关基因与氧化还原敏感蛋白质的响应变化。基于此构建免疫应答调控网络，阐明PBDEs毒性效应的分子生物学机理。

Persistent organic pollutants (POPs) result in the imbalance of coastal ecosystem damage the ecological functions and reduce the ecological services. A new class of POPs, polybrominated flame retardants (PBDEs), is paid much attention in the last decade because of its increasingly and negatively ecological impacts, especially on benthic ecosystem. In the present project, we emphasize on the benthic sentinel organism, blue mussel Mytilus edulis, and innovative studies on the immune trade-off strategy and immune-responding mechanisms induced by PBDEs are discussed in haemocytes of M. edulis. Two hypotheses are proposed and are explained in the present project. First is “the immune responses could be traded off according to the environmental changes, and this trade-off strategy is plastic”. To prove it, the changes of immune functions and immune energy cost would be analyzed, and the trade off strategy and its environmental plastics would be elucidated from views of cellular growth, immune function, energy cost, environmental changes and their interactions. The other question is “the key immune-responding genes and redox-sensitive proteins play pivotal roles in immune responses in haemocytes of M. edulis to PBDEs”. To prove it, the combination of new techniques based on redox proteomics and comparative transcriptomic would be utilized to high-throughput and complementarily analyze their responding differentiations when exposed to different stressing conditions. These responding differentiations are suggested to be involved in the key processes of immune responses. The regulating network would be established to the toxicity induced by PBDEs.