The immunology of stroke: from mechanisms to translation

By C. Iadecola, J. Anrather. Nature Medicine, 2011

2,442 citations recorded by the source corpus.

Immunity and inflammation are key elements of the pathobiology of stroke, a devastating illness second only to cardiac ischemia as a cause of death worldwide. While the immune system participates in the brain damage produced by ischemia, the damaged brain, in turn, exerts a powerful immunosuppressive effect that promotes fatal intercurrent infections and threatens the survival of stroke patients. Inflammatory signaling is instrumental in all stages of the ischemic cascade, from the early damaging events triggered by arterial occlusion, to the late regenerative processes underlying post-ischemic tissue repair. Recent developments have revealed that stroke, like multiple sclerosis, engages both innate and adaptive immunity. But, unlike multiple sclerosis, adaptive immunity triggered by newly exposed brain antigens does not have an impact on the acute phase of the damage. Nevertheless, modulation of adaptive immunity exerts a remarkable protective effect on the ischemic brain and offers the prospect of new stroke therapies. However, immunomodulation is not devoid of deleterious side effects, and gaining a better understanding of the reciprocal interaction between the immune system and the ischemic brain is essential to harness the full therapeutic potential of the immunology of stroke.

Subfields: Immunology, Neurology

View Paper: https://www.semanticscholar.org/paper/89c741eaabdba2c197b1c644c1908fee8201100f

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In Immunology

1. C. Iadecola
2. Guo-Yuan Yang
3. Yongting Wang
4. Jixian Wang
5. Yuanyuan Ma
6. J. Anrather
7. Liang Liu
8. Qing-Wu Yang

In Neurology

1. C. Iadecola
2. Guo-Yuan Yang
3. Yongting Wang
4. Jixian Wang
5. Yuanyuan Ma
6. Martin Dichgans
7. J. Anrather
8. Liang Liu

Citations in the corpus

• Microbiota Dysbiosis Controls the Neuroinflammatory Response after Stroke (2016, background): “…a key role for differential Thelper cell priming in stroke pathophysiology, in which proinflammatory Th1, Th17, and T cells deteriorate poststroke inflammation, whereas Treg cells limit the inflammatory collateral damage (Shichita et al., 2009; Iadecola and Anrather, 2011; Chamorro et al., 2012).”
• Immune responses to stroke: mechanisms, modulation, and therapeutic potential. (2020, background): “In the past, several clinical trials attempted to target postischemic immune responses with disappointing results, in part due to an incomplete understanding of poststroke immunity (19).”
• Mechanisms of neuronal cell death in ischemic stroke and their therapeutic implications (2021, background): “manifest themselves days or weeks after ischemia, the inflammation cascade is activated immediately after a blood vessel is blocked.(61,62) In rodent models of ischemic stroke, early activation of resident microglia activates the”
• The pathobiology of vascular dementia (2013, positive): “In conditions of hypoxia-ischemia, endothelial cells express adhesion receptors, such as P-selectin, E-selectin, ICAM, and VCAM, instrumental for the transfer of circulating leukocytes into the perivascular space (Iadecola and Anrather, 2011).”
• The biphasic function of microglia in ischemic stroke (2017, positive): “, 2009), anti-inflammatory cytokines (such as TGF-b) (Iadecola and Anrather, 2011), growth and trophic factors such as insulinlike growth factor 1 (IGF-1), basic fibroblast growth factor (bFGF), hepatocyte growth factor (HGF), platelet-derived growth factor (PDGF) (Lai and Todd, 2006), nerve growth ”
• Inflammation and Stroke: An Overview (2016, background): “event, the inflammatory cascade is activated immediately after vessel occlusion has occurred [5, 6].”
• Mitochondrial dysfunction: mechanisms and advances in therapy (2024, background): “204,209 ROS contributes to cell and tissue impairment through lipid peroxidation within cell membranes and organelles, DNA oxidation, and the activation of matrix metalloproteinases and calpains.”
• Acute cerebrovascular disease following COVID-19: a single center, retrospective, observational study (2020, background): “Physicians should pay more attention to controlling risk factors for CVDs, such as hypertension, high coagulation state and diabetes mellitus while treating the older or severe patients with COVID-19.”
• Post-stroke infection: A systematic review and meta-analysis (2011, background): “Evidence from experimental studies suggests that infection promotes antigen presentation and autoimmunity against the brain [41].”
• Signaling pathways involved in ischemic stroke: molecular mechanisms and therapeutic interventions (2022, background): “During the whole process of inflammation, various immune cells including microglia, macrophages, and T lymphocytes are activated.(216,217) Also, the production of inflammation-related cytokines are stimulated, as well as interferons or chemokines including monocyte chemoattractant protein-1 (MCP-1).”
• Functions and mechanisms of microglia/macrophages in neuroinflammation and neurogenesis after stroke. (2016, background): “The immune system is considered to play a significant role in determining the condition of the brain and the survival of patients following stroke (Iadecola and Anrather, 2011).”