Neuroinflammation contributes substantially to stroke pathophysiology. Cerebral invasion of peripheral leukocytes—particularly T cells—has been shown to be a key event promoting inflammatory tissue damage after stroke. While previous research has focused on the vascular invasion of T cells into the ischemic brain, the choroid plexus (ChP) as an alternative cerebral T-cell invasion route after stroke has not been investigated. We here report specific accumulation of T cells in the peri-infarct cortex and detection of T cells as the predominant population in the ipsilateral ChP in mice as well as in human post-stroke autopsy samples. T-cell migration from the ChP to the peri-infarct cortex was confirmed by in vivo cell tracking of photoactivated T cells. In turn, significantly less T cells invaded the ischemic brain after photothrombotic lesion of the ipsilateral ChP and in a stroke model encompassing ChP ischemia. We detected a gradient of CCR2 ligands as the potential driving force and characterized the neuroanatomical pathway for the intracerebral migration. In summary, our study demonstrates that the ChP is a key invasion route for post-stroke cerebral T-cell invasion and describes a CCR2-ligand gradient between cortex and ChP as the potential driving mechanism for this invasion route.

神经炎症实质上有助于中风的病理生理。大脑对周围白细胞（尤其是T细胞）的侵袭已被证明是促进卒中后炎性组织损伤的关键事件。尽管先前的研究集中于T细胞在缺血性脑中的血管浸润，但尚未研究卒中后脉络丛（ChP）作为大脑T细胞的另一种浸润途径。我们在这里报告了T细胞在梗死周围皮层中的特异性积累，并在小鼠以及人类中风后尸检样本中检测到T细胞作为同侧ChP中的主要种群。T细胞从ChP迁移到梗死周围皮层的过程已通过体内对光活化T细胞的细胞追踪得到证实。反过来，在同侧ChP发生光血栓形成病变后，在包含ChP缺血的中风模型中，侵袭缺血性脑的T细胞明显减少。我们检测到CCR2配体的梯度作为潜在的驱动力，并表征了脑内迁移的神经解剖学途径。总而言之，我们的研究表明ChP是中风后脑T细胞入侵的关键入侵途径，并将皮质和ChP之间的CCR2配体梯度描述为该入侵途径的潜在驱动机制。