Mathias Khiany, Machado Richard Simon, Tiscoski Anita Dal Bó, Dos Santos David, Lippert Fabricio Weinheimer, Costa Maiara Aguiar, Gonçalves Cinara Ludvig, Generoso Jaqueline Silva, Prophiro Josiane Somariva, Giustina Amanda Della, Petronilho Fabricia
Laboratory of Experimental Neurology, Health Sciences Unit, Graduate Program in Health Sciences, University of Southern Santa Catarina, Criciuma, SC, Brazil.
Health Sciences Unit, Program in Health Sciences, University of South Santa Catarina, Tubarao, SC, Brazil.
Inflammation. 2024 Sep 19. doi: 10.1007/s10753-024-02148-6.
Cerebrovascular disease is the second-leading cause of death and disability worldwide, with stroke being the most common cause. In ischemic stroke, several processes combine to produce immunosuppression, leaving the post-stroke body susceptible to infection, which in turn affects neuroinflammation. Interleukin-33 (IL-33), a member of the interleukin-1 family (IL-1), functions as a modulator of immune responses and inflammation, playing a crucial role in the establishment of immunologic responses. IL-33 has been shown to have a protective effect on brain injury and represents a potential target by modulating inflammatory cytokines and stimulating immune regulatory cells. With an emphasis on preclinical and clinical studies, this review covers the impact of IL-33 on immune system mechanisms following ischemic stroke.
脑血管疾病是全球第二大致死和致残原因,中风是最常见的病因。在缺血性中风中,多种过程共同作用导致免疫抑制,使中风后的机体易受感染,进而影响神经炎症。白细胞介素-33(IL-33)是白细胞介素-1家族(IL-1)的成员之一,作为免疫反应和炎症的调节剂,在免疫反应的建立中起关键作用。IL-33已被证明对脑损伤具有保护作用,并且通过调节炎性细胞因子和刺激免疫调节细胞而成为一个潜在靶点。本综述着重于临床前和临床研究,涵盖了IL-33对缺血性中风后免疫系统机制的影响。