天津医科大学最新Science论文：施福东发现团队抑制大脑炎症及神经退行的新靶点，开辟神经疾病治疗新路径

Core Viewpoint - The research identifies FPR1 signaling as a potential mechanism for the progression of Multiple Sclerosis (MS), suggesting that FPR1 could serve as a new therapeutic target for MS treatment [2][3]. Group 1: Research Findings - The study published in Science highlights the development of the FPR1 small molecule antagonist T0080, which can reduce brain inflammation and neurodegeneration, thereby alleviating the progression of MS [3]. - In active MS, the presence of reactive microglia and macrophages contributes to the development of tissue-restrictive inflammation, leading to progressive tissue damage and exacerbating neurodegeneration [5]. - The research team found significant expression of FPR1 in microglia and infiltrating macrophages in MS patients, with levels of endogenous N-formyl peptides correlating dynamically with disease progression [5][6]. Group 2: Mechanism of Action - Activation of FPR1 initiates a PKC-dependent signaling cascade, leading to the release of reactive oxygen species (ROS) and inflammatory cytokines like TNF-α, which damages neuronal axons and promotes a neuroinflammatory environment [6]. - The study demonstrates that FPR1-expressing microglia secrete CCL5, facilitating the recruitment and clonal expansion of myelin-reactive CD4+ T cells, which further amplifies myelin destruction and neuroinflammation [6][8]. Group 3: Implications for Treatment - The findings suggest that targeting FPR1 with the antagonist T0080 may have therapeutic potential in slowing the progression of MS, as it has shown efficacy in various MS mouse models by mitigating autoimmune responses and inhibiting microglia-mediated axonal degeneration [6][8].