Department of Neurology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Front Immunol. 2019 Apr 2;10:686. doi: 10.3389/fimmu.2019.00686. eCollection 2019.
Ischemic Stroke is a major cause of morbidity and mortality worldwide. Sterile inflammation occurs after both stroke subtypes and contributes to neuronal injury and damage to the blood-brain barrier with release of brain antigens and a potential induction of autoimmune responses that escape central and peripheral tolerance mechanisms. In stroke patients, the detection of T cells and antibodies specific to neuronal antigens suggests a role of humoral adaptive immunity. In experimental models stroke leads to a significant increase of autoreactive T and B cells to CNS antigens. Lesion volume and functional outcome in stroke patients and murine stroke models are connected to antigen-specific responses to brain proteins. In patients with traumatic brain injury (TBI) a range of antibodies against brain proteins can be detected in serum samples. In this review, we will summarize the role of autoimmunity in post-lesional conditions and discuss the role of B and T cells and their potential neuroprotective or detrimental effects.
缺血性脑卒中是全球范围内发病率和死亡率的主要原因。两种脑卒中亚型都会发生无菌性炎症，导致神经元损伤和血脑屏障损伤，释放脑抗原，并可能引发自身免疫反应，从而逃避中枢和外周耐受机制。在脑卒中患者中，T 细胞和针对神经元抗原的抗体的检测提示体液适应性免疫的作用。在实验模型中，脑卒中导致对中枢神经系统抗原的自身反应性 T 和 B 细胞显著增加。脑卒中患者和小鼠脑卒中模型的病变体积和功能结果与针对脑蛋白的抗原特异性反应有关。在创伤性脑损伤（TBI）患者中，可以在血清样本中检测到针对脑蛋白的一系列抗体。在这篇综述中，我们将总结自身免疫在损伤后状态中的作用，并讨论 B 和 T 细胞的作用及其潜在的神经保护或有害作用。
