Abstract
Although the primary responsibility of the immune system has for over a century been perceived as the protector of the host against infection in the peripheral organs, we now know the immune system also plays a vital role in recovery pathways associated with central nervous system (CNS) injury. There is mounting evidence that the blood–brain barrier does not preclude the CNS from immune surveillance. Of particular interest for this review is how microglia and astrocytes interact with the cells of the immune system to modulate repair and recovery mechanisms in ischemic stroke. Our review argues that by deepening our understanding of neuroimmunity, specifically the bidirectional glial–immune cell communications, a plethora of new therapeutic targets and mechanisms may be revealed. Consequently, this review instigates novel experimental approaches to neuroimmunology and fosters a more rapid discovery process for the treatment of stroke. Impact statement: This article reviews glial cell interactions with the immune system post-ischemic stroke. Research has shown that glial cells in the brain play a role in altering phenotypes of other glial cells and have downstream immune cell targets ultimately regulating a neuroinflammatory response. These interactions may play a deleterious as well as beneficial role in stroke recovery. Furthermore, they may provide a novel way to approach potential therapies, since current stroke drug therapy is limited to only one Food and Drug Administration-approved drug complicated by a narrow therapeutic window. Until this point, most research has emphasized neuroimmune interactions, but little focus has been on bidirectional communication of glial–immune interactions in the ischemic brain. By expanding our understanding of these interactions through a compilation of glial cell effects, we may be able to pinpoint major modulating factors in brain homeostasis to maintain or discover ways to suppress irreversible ischemic damage and improve brain repair.
| Original language | English |
|---|---|
| Pages (from-to) | 1302-1312 |
| Number of pages | 11 |
| Journal | Experimental Biology and Medicine |
| Volume | 243 |
| Issue number | 17-18 |
| DOIs | |
| State | Published - 1 Dec 2018 |
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Keywords
- Ischemic stroke
- T-cells
- astrocytes
- glial–immune interactions
- glutamate
- histamine
- interleukin-15
- microglia
- monocytes
- natural killer cells
- neuroimmunology
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Glia–immune interactions post-ischemic stroke and potential therapies. / Hersh, Jessica; Yang, Shao Hua.
In: Experimental Biology and Medicine, Vol. 243, No. 17-18, 01.12.2018, p. 1302-1312.Research output: Contribution to journal › Review article
TY - JOUR
T1 - Glia–immune interactions post-ischemic stroke and potential therapies
AU - Hersh, Jessica
AU - Yang, Shao Hua
PY - 2018/12/1
Y1 - 2018/12/1
N2 - Although the primary responsibility of the immune system has for over a century been perceived as the protector of the host against infection in the peripheral organs, we now know the immune system also plays a vital role in recovery pathways associated with central nervous system (CNS) injury. There is mounting evidence that the blood–brain barrier does not preclude the CNS from immune surveillance. Of particular interest for this review is how microglia and astrocytes interact with the cells of the immune system to modulate repair and recovery mechanisms in ischemic stroke. Our review argues that by deepening our understanding of neuroimmunity, specifically the bidirectional glial–immune cell communications, a plethora of new therapeutic targets and mechanisms may be revealed. Consequently, this review instigates novel experimental approaches to neuroimmunology and fosters a more rapid discovery process for the treatment of stroke. Impact statement: This article reviews glial cell interactions with the immune system post-ischemic stroke. Research has shown that glial cells in the brain play a role in altering phenotypes of other glial cells and have downstream immune cell targets ultimately regulating a neuroinflammatory response. These interactions may play a deleterious as well as beneficial role in stroke recovery. Furthermore, they may provide a novel way to approach potential therapies, since current stroke drug therapy is limited to only one Food and Drug Administration-approved drug complicated by a narrow therapeutic window. Until this point, most research has emphasized neuroimmune interactions, but little focus has been on bidirectional communication of glial–immune interactions in the ischemic brain. By expanding our understanding of these interactions through a compilation of glial cell effects, we may be able to pinpoint major modulating factors in brain homeostasis to maintain or discover ways to suppress irreversible ischemic damage and improve brain repair.
AB - Although the primary responsibility of the immune system has for over a century been perceived as the protector of the host against infection in the peripheral organs, we now know the immune system also plays a vital role in recovery pathways associated with central nervous system (CNS) injury. There is mounting evidence that the blood–brain barrier does not preclude the CNS from immune surveillance. Of particular interest for this review is how microglia and astrocytes interact with the cells of the immune system to modulate repair and recovery mechanisms in ischemic stroke. Our review argues that by deepening our understanding of neuroimmunity, specifically the bidirectional glial–immune cell communications, a plethora of new therapeutic targets and mechanisms may be revealed. Consequently, this review instigates novel experimental approaches to neuroimmunology and fosters a more rapid discovery process for the treatment of stroke. Impact statement: This article reviews glial cell interactions with the immune system post-ischemic stroke. Research has shown that glial cells in the brain play a role in altering phenotypes of other glial cells and have downstream immune cell targets ultimately regulating a neuroinflammatory response. These interactions may play a deleterious as well as beneficial role in stroke recovery. Furthermore, they may provide a novel way to approach potential therapies, since current stroke drug therapy is limited to only one Food and Drug Administration-approved drug complicated by a narrow therapeutic window. Until this point, most research has emphasized neuroimmune interactions, but little focus has been on bidirectional communication of glial–immune interactions in the ischemic brain. By expanding our understanding of these interactions through a compilation of glial cell effects, we may be able to pinpoint major modulating factors in brain homeostasis to maintain or discover ways to suppress irreversible ischemic damage and improve brain repair.
KW - Ischemic stroke
KW - T-cells
KW - astrocytes
KW - glial–immune interactions
KW - glutamate
KW - histamine
KW - interleukin-15
KW - microglia
KW - monocytes
KW - natural killer cells
KW - neuroimmunology
UR - http://www.scopus.com/inward/record.url?scp=85060578543&partnerID=8YFLogxK
U2 - 10.1177/1535370218818172
DO - 10.1177/1535370218818172
M3 - Review article
C2 - 30537868
AN - SCOPUS:85060578543
VL - 243
SP - 1302
EP - 1312
JO - Experimental Biology and Medicine
JF - Experimental Biology and Medicine
SN - 1535-3702
IS - 17-18
ER -