快感缺失是精神分裂症阴性症状的核心表现，指对快乐的体验能力下降，严重影响患者的社会功能和预后。这种异常情感体验的神经机制在于前额叶多巴胺能不足。既往研究显示精神分裂症患者存在多种免疫功能异常，补体作为免疫调节单位与阴性症状之间存在重要联系。补体因子H（CFH）是补体激活途径的调控因子。我们在前期研究中发现CFH基因对精神分裂症阴性症状严重程度影响显著。此外，我们还发现CFH基因可能通过调控脑内神经免疫反应影响情感体验过程。因此，本研究假设CFH可能通过介导炎症反应影响精神分裂症患者前额叶多巴胺能神经元引起多巴胺能低下，导致患者出现快感缺失。在本研究中，我们通过临床和前临床研究，分别从临床表型、行为学和分子生物学等多个层面探索CFH在精神分裂症快感缺失中的作用和机制，期望发现快感缺失表型新的分子靶点，对于精神分裂症的临床干预、康复治疗以及新药研发具有重要的理论价值和现实意义。

Anhedonia is the core feature of negative symptoms in schizophrenia. It means the diminished capacity to experience pleasure and causes serous effect on the social function and prognosis in patients with schizophrenia. The mechanism of such aberrant emotional experience lies in lack of dopaminergic release in prefrontal cortex. Previous studies showed that schizophrenia patients have many abnormal immune responses. Complement acts as a key system for immune regulation and has implication with negative symptoms in schizophrenia. Complement factor H (CFH) is the modulation factor in complement activation pathway. Our previous study showed that CFH gene influences the severity of negative symptoms in schizophrenia. Additionally, we found that CFH gene may influence the emotional experience through modulating immune responses in brain. Therefore, we hypothesized that CFH may decrease domapinergic release through neuroinflammation response and lead to anhedonia in patients with schizophrenia. In this study, we conducted a clinical and preclinical study to explore the effect and mechanism of CFH on anhedonia in schizophrenia from the levels of clinical features, behavior and molecular biology, aiming to find the novel molecular target of anhedonia. This study has important theoretical and practical value in clinical intervention, rehabilitation therapy and drug discovery.