摘要创伤性脑损伤（TBI）是导致暂时或永久性运动、认知功能障碍的主要原因。TBI会引发大脑中的炎症反应，以促进细胞碎片清除和组织修复。然而，免疫细胞过度和长期激活会放大炎症级联反应，加剧神经元损伤或死亡，并可能导致严重的脑功能障碍或退行性疾病。因此，持续性炎症引起的继发性损伤是TBI病理过程的关键组成部分。乳酸作为无氧糖酵解的主要代谢产物，TBI后其浓度明显升高，并作为重要的免疫调控分子而非代谢废物参与脑内炎症反应。特别重要的是，组蛋白乳酸化作为乳酸衍生的新型组蛋白翻译后修饰（HPTM）方式，允许乳酸参与调控中枢神经系统的复杂病理生理学过程。因此，深入研究TBI时组蛋白乳酸化作用过程及其免疫调控机制，有望为早期干预并改善TBI患者预后提供新的见解。为此，笔者就组蛋白乳酸化在TBI免疫调控中作用的研究进展进行综述，从HPTM角度为进一步阐明TBI致伤机制、探寻新的预警和诊治措施提供借鉴。

abstractsTraumatic brain injury (TBI) is a major reason for temporary or permanent dyskinesia and cognitive impairment of the organism. Generally, TBI induces subsequent neuroinflammation to assist cell debris removal and tissue repair and regeneration after injury. However, overactivation or long-term activation of immune cells will exacerbate nerve damage or death, cause cognitive dysfunction, and ultimately lead to neurodegenerative diseases. Therefore, secondary damage caused by persistent inflammation is a key component of TBI pathological process. As the main metabolite of anaerobic glycolysis, lactate is increased after TBI and participates in brain inflammation as an important immune regulatory molecule rather than a metabolic waste. Importantly, histone lysine lactylation as a novel type of histone post-translational modifications (HPTM) derived from lactate allows lactate to participate in the regulation of complex immunopathophysiological processes of the central nervous system after TBI. Further study on the process of histone lactylation and its immune regulation mechanism during TBI may provide new insights for early intervention and improvement of TBI prognosis. Thus, the authors reviewed the role of histone lactylation in the immune regulation of TBI, so as to further elucidate the mechanism of TBI and the explore new warning and prevention measures from the perspective of HPTM.