2018/11/27 by Kate Lykke Lambertsen, Bente Finsen, Bettina Hjelm Clausen · 472 citations
Immunology and Microbiology · Medicine · Neuroscience · #Acute Ischemic Stroke Management #Biology #Immune Response and Inflammation #Immune system #Immunology #Inflammation #Internal medicine #Medicine #Microglia #Neuroinflammation and Neurodegeneration Mechanisms #Neuroprotection #Neuroscience #Stroke (engine) #Tumor necrosis factor alpha
paper · pdf · doi:10.1007/s00401-018-1930-z
published in Acta Neuropathologica 137(5), 693-714 (Springer Science+Business Media)
openalex publication_date 2018/11/27 · openalex created_date 2025/10/10 · openalex updated_date 2026/08/05
Inflammation is currently considered a prime target for the development of new stroke therapies. In the acute phase of ischemic stroke, microglia are activated and then circulating immune cells invade the peri-infarct and infarct core. Resident and infiltrating cells together orchestrate the post-stroke inflammatory response, communicating with each other and the ischemic neurons, through soluble and membrane-bound signaling molecules, including cytokines. Inflammation can be both detrimental and beneficial at particular stages after a stroke. While it can contribute to expansion of the infarct, it is also responsible for infarct resolution, and influences remodeling and repair. Several pre-clinical and clinical proof-of-concept studies have suggested the effectiveness of pharmacological interventions that target inflammation post-stroke. Experimental evidence shows that targeting certain inflammatory cytokines, such as tumor necrosis factor, interleukin (IL)-1, IL-6, and IL-10, holds promise. However, as these cytokines possess non-redundant protective and immunoregulatory functions, their neutralization or augmentation carries a risk of unwanted side effects, and clinical translation is, therefore, challenging. This review summarizes the cell biology of the post-stroke inflammatory response and discusses pharmacological interventions targeting inflammation in the acute phase after a stroke that may be used alone or in combination with recanalization therapies. Development of next-generation immune therapies should ideally aim at selectively neutralizing pathogenic immune signaling, enhancing tissue preservation, promoting neurological recovery and leaving normal function intact.