Effect of experimental stroke on peripheral immunity

CNS ischemia induces profound immunosuppression

Research output: Contribution to journalArticle

140 Citations (Scopus)

Abstract

The profound damage to the CNS caused by ischemic lesions has been well documented. Yet, relatively little is known about the contribution to and effects on the immune system during stroke. We have focused on both early and late events in the peripheral immune system during stroke in mice and have observed an early activation of splenocytes that conceivably could result in immune-mediated damage in the developing CNS lesion, followed by global immunosuppression that affects the spleen, thymus, lymph nodes and circulation. While this second immunosuppressive phase may not directly enhance infarction size, it without doubt leads to an inability to respond to antigenic challenges, thereby enhancing the risk for crippling systemic infection and septicemia in stroke survivors. These novel findings advocate the need to develop or effectively utilize agents that can block early neural splenic activation and modulate immune cells specific for brain antigens as a means to prevent mobilization of T and B cells carrying a cytokine death warrant to the brain. Equally important for the recovering stroke patient are approaches that can derail the second phase of immune dysfunction and restore the ability to mount a defense against systemic infectious insults.

Original languageEnglish (US)
Pages (from-to)1098-1111
Number of pages14
JournalNeuroscience
Volume158
Issue number3
DOIs
StatePublished - Feb 6 2009

Fingerprint

Immunosuppression
Immunity
Ischemia
Stroke
Immune System
Brain
Immunosuppressive Agents
Infarction
Thymus Gland
Survivors
Sepsis
B-Lymphocytes
Spleen
Lymph Nodes
Cytokines
T-Lymphocytes
Antigens
Infection

Keywords

  • immunosuppression
  • macrophages
  • spleen
  • stroke
  • Treg cells

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Effect of experimental stroke on peripheral immunity : CNS ischemia induces profound immunosuppression. / Offner, Halina; Vandenbark, Arthur; Hurn, P. D.

In: Neuroscience, Vol. 158, No. 3, 06.02.2009, p. 1098-1111.

Research output: Contribution to journalArticle

@article{500d858ff4f24d9ebc0c30783cde2941,
title = "Effect of experimental stroke on peripheral immunity: CNS ischemia induces profound immunosuppression",
abstract = "The profound damage to the CNS caused by ischemic lesions has been well documented. Yet, relatively little is known about the contribution to and effects on the immune system during stroke. We have focused on both early and late events in the peripheral immune system during stroke in mice and have observed an early activation of splenocytes that conceivably could result in immune-mediated damage in the developing CNS lesion, followed by global immunosuppression that affects the spleen, thymus, lymph nodes and circulation. While this second immunosuppressive phase may not directly enhance infarction size, it without doubt leads to an inability to respond to antigenic challenges, thereby enhancing the risk for crippling systemic infection and septicemia in stroke survivors. These novel findings advocate the need to develop or effectively utilize agents that can block early neural splenic activation and modulate immune cells specific for brain antigens as a means to prevent mobilization of T and B cells carrying a cytokine death warrant to the brain. Equally important for the recovering stroke patient are approaches that can derail the second phase of immune dysfunction and restore the ability to mount a defense against systemic infectious insults.",
keywords = "immunosuppression, macrophages, spleen, stroke, Treg cells",
author = "Halina Offner and Arthur Vandenbark and Hurn, {P. D.}",
year = "2009",
month = "2",
day = "6",
doi = "10.1016/j.neuroscience.2008.05.033",
language = "English (US)",
volume = "158",
pages = "1098--1111",
journal = "Neuroscience",
issn = "0306-4522",
publisher = "Elsevier Limited",
number = "3",

}

TY - JOUR

T1 - Effect of experimental stroke on peripheral immunity

T2 - CNS ischemia induces profound immunosuppression

AU - Offner, Halina

AU - Vandenbark, Arthur

AU - Hurn, P. D.

PY - 2009/2/6

Y1 - 2009/2/6

N2 - The profound damage to the CNS caused by ischemic lesions has been well documented. Yet, relatively little is known about the contribution to and effects on the immune system during stroke. We have focused on both early and late events in the peripheral immune system during stroke in mice and have observed an early activation of splenocytes that conceivably could result in immune-mediated damage in the developing CNS lesion, followed by global immunosuppression that affects the spleen, thymus, lymph nodes and circulation. While this second immunosuppressive phase may not directly enhance infarction size, it without doubt leads to an inability to respond to antigenic challenges, thereby enhancing the risk for crippling systemic infection and septicemia in stroke survivors. These novel findings advocate the need to develop or effectively utilize agents that can block early neural splenic activation and modulate immune cells specific for brain antigens as a means to prevent mobilization of T and B cells carrying a cytokine death warrant to the brain. Equally important for the recovering stroke patient are approaches that can derail the second phase of immune dysfunction and restore the ability to mount a defense against systemic infectious insults.

AB - The profound damage to the CNS caused by ischemic lesions has been well documented. Yet, relatively little is known about the contribution to and effects on the immune system during stroke. We have focused on both early and late events in the peripheral immune system during stroke in mice and have observed an early activation of splenocytes that conceivably could result in immune-mediated damage in the developing CNS lesion, followed by global immunosuppression that affects the spleen, thymus, lymph nodes and circulation. While this second immunosuppressive phase may not directly enhance infarction size, it without doubt leads to an inability to respond to antigenic challenges, thereby enhancing the risk for crippling systemic infection and septicemia in stroke survivors. These novel findings advocate the need to develop or effectively utilize agents that can block early neural splenic activation and modulate immune cells specific for brain antigens as a means to prevent mobilization of T and B cells carrying a cytokine death warrant to the brain. Equally important for the recovering stroke patient are approaches that can derail the second phase of immune dysfunction and restore the ability to mount a defense against systemic infectious insults.

KW - immunosuppression

KW - macrophages

KW - spleen

KW - stroke

KW - Treg cells

UR - http://www.scopus.com/inward/record.url?scp=59349116941&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=59349116941&partnerID=8YFLogxK

U2 - 10.1016/j.neuroscience.2008.05.033

DO - 10.1016/j.neuroscience.2008.05.033

M3 - Article

VL - 158

SP - 1098

EP - 1111

JO - Neuroscience

JF - Neuroscience

SN - 0306-4522

IS - 3

ER -