Coordination Funds

在工业化国家，缺血性中风是导致长期残疾的主要原因，也是导致死亡的第三大原因。目前中风的治疗方法有限，临床前实验结果在临床试验中往往失败。因此，迫切需要具有高翻译潜力的基础研究的新途径，以开发有效的治疗策略。虽然脑缺血局部炎症过程的发展是一个已知的现象，但这些免疫过程是如何与梗死区的二次扩大联系在一起的，以及免疫系统在中风后再生中的作用仍然知之甚少。有趣的是，虽然脑缺血传统上不被认为是典型的神经炎症性疾病，但中风会引发过多的免疫反应，类似于自身免疫性脑部疾病的反应。此外，中风相关的急性脑损伤对外周免疫系统有强大的影响，诱导多相免疫反应。免疫反应和脑损伤之间的相互作用还知之甚少，特别是关于中风后康复的潜在机制。该研究单位免疫中风专注于研究免疫在中风后修复机制和长期康复中的作用。为在第二个资助期更新该联盟而描述的项目旨在：i)解决免疫如何调节中风后的康复过程；ii)阐明中风患者神经炎症的作用；iii)并确定中风后神经炎的新标记物。这些目标将利用尖端技术和新的治疗范例来实现，以了解和调节实验性中风后发生的免疫反应。重要的是，临床前实验将高度标准化，关键发现将在多中心临床前随机对照试验中得到验证，这些实验将得到使用中风患者进行的分析的支持。

Ischemic stroke is the primary cause of long-term disability and the third leading cause of death in industrialized countries. Current treatments for stroke are limited, and preclinical experimental findings often fail in clinical trials. Therefore, new avenues of basic research with high translation potential are desperately needed in order to develop effective therapeutic strategies. Although the development of local inflammatory processes in the ischemic brain is a known phenomenon, precisely how these immune processes are linked to the secondary expansion of the infarct area and the role of the immune system in post-stroke regeneration remain poorly understood. Interestingly, while cerebral ischemia is traditionally not considered a classic neuroinflammatory disorder, stroke induces a plethora of immune responses similar to the responses that occur in autoimmune brain diseases. Moreover, the stroke-related acute brain injury has a robust effect on the peripheral immune system, inducing a multiphasic immune response. The reciprocal interaction between immunological responses and brain injury is poorly understood, particularly with respect to the mechanisms underlying recovery following stroke. This research unit ImmunoStroke is focusing on studying the role of immunity in repair mechanisms and long-term recovery following stroke. The projects described for the renewal of this consortium in its second funding period are designed to i) address how immunity modulates the recovery process following stroke; ii) clarify the role of neuroinflammation in stroke patients; and iii) and identify novel markers of post-stroke neuroinflammation. These goals will be achieved using cutting-edge technologies and new treatment paradigms in order to understand and modulate the immune responses that occur following experimental stroke. Importantly, the preclinical experiments will be highly standardized, the key findings will be validated in multicenter preclinical RCTs, and the experiments will be supported by analyses performed using stroke patients.