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Brain-Immune Interactions and Ischemic Stroke

Brain-Immune Interactions and Ischemic Stroke NEUROLOGICAL REVIEW Clinical Implications Hooman Kamel, MD; Costantino Iadecola, MD ncreasing evidence shows that the central nervous system and the immune system interact in complex ways, and better insight into these interactions may be relevant to the treat- ment of patients with stroke and other forms of central nervous system injury. Atheroscle- I rosis, autoimmune disease, and physiological stressors, such as infection or surgery, cause inflammation that contributes to vascular injury and increases the risk of stroke. In addition, the immune system actively participates in the acute pathogenesis of stroke. Thrombosis and hypoxia trigger an intravascular inflammatory cascade, which is further augmented by the innate immune response to cellular damage occurring in the parenchyma. This immune activation may cause sec- ondary tissue injury, but it is unclear whether modulating the acute immune response to stroke can produce clinical benefits. Attempts to dampen immune activation after stroke may have ad- verse effects because central nervous system injury causes significant immunodepression that places patients at higher risk of infections, such as pneumonia. The activation of innate immunity after stroke sets the stage for an adaptive immune response directed against brain antigens. The patho- genic significance of adaptive immunity and its long-term http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png JAMA Neurology American Medical Association

Brain-Immune Interactions and Ischemic Stroke

Kamel, Hooman; Iadecola, Costantino
JAMA Neurology , Volume 69 (5) – May 1, 2012
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References (10)

Publisher
American Medical Association
Copyright
Copyright 2012 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.
ISSN
2168-6149
eISSN
2168-6157
DOI
10.1001/archneurol.2011.3590
pmid
22782509
Publisher site
See Article on Publisher Site

Abstract

NEUROLOGICAL REVIEW Clinical Implications Hooman Kamel, MD; Costantino Iadecola, MD ncreasing evidence shows that the central nervous system and the immune system interact in complex ways, and better insight into these interactions may be relevant to the treat- ment of patients with stroke and other forms of central nervous system injury. Atheroscle- I rosis, autoimmune disease, and physiological stressors, such as infection or surgery, cause inflammation that contributes to vascular injury and increases the risk of stroke. In addition, the immune system actively participates in the acute pathogenesis of stroke. Thrombosis and hypoxia trigger an intravascular inflammatory cascade, which is further augmented by the innate immune response to cellular damage occurring in the parenchyma. This immune activation may cause sec- ondary tissue injury, but it is unclear whether modulating the acute immune response to stroke can produce clinical benefits. Attempts to dampen immune activation after stroke may have ad- verse effects because central nervous system injury causes significant immunodepression that places patients at higher risk of infections, such as pneumonia. The activation of innate immunity after stroke sets the stage for an adaptive immune response directed against brain antigens. The patho- genic significance of adaptive immunity and its long-term

Journal

JAMA Neurology – American Medical Association

Published: May 1, 2012

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