Exploring the role of interleukin-27 as a regulator of neuronal survival in central nervous system diseases
Interleukin-27 is a pleiotropic cytokine that is involved in tissue responses to infection, cell stress, neuronal disease, and tumors. Recent studies in various tissues indicate that interleukin-27 has complex activating and inhibitory properties in innate and acquired immunity. The availability of...
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Format: | Article |
Language: | English |
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Wolters Kluwer Medknow Publications
2022-01-01
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Series: | Neural Regeneration Research |
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Online Access: | http://www.nrronline.org/article.asp?issn=1673-5374;year=2022;volume=17;issue=10;spage=2149;epage=2152;aulast= |
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author | Andrea N Nortey Kimberly N Garces Abigail S Hackam |
author_facet | Andrea N Nortey Kimberly N Garces Abigail S Hackam |
author_sort | Andrea N Nortey |
collection | DOAJ |
description | Interleukin-27 is a pleiotropic cytokine that is involved in tissue responses to infection, cell stress, neuronal disease, and tumors. Recent studies in various tissues indicate that interleukin-27 has complex activating and inhibitory properties in innate and acquired immunity. The availability of recombinant interleukin-27 protein and mice with genetic deletions of interleukin-27, its receptors and signaling mediators have helped define the role of interleukin-27 in neurodegenerative diseases. Interleukin-27 has been well-characterized as an important regulator of T cell activation and differentiation that enhances or suppresses T cell responses in autoimmune conditions in the central nervous system. Evidence is also accumulating that interleukin-27 has neuroprotective activities in the retina and brain. Interleukin-27 is secreted from and binds to infiltrating microglia, macrophage, astrocytes, and even neurons and it promotes neuronal survival by regulating pro- and anti-inflammatory cytokines, neuroinflammatory pathways, oxidative stress, apoptosis, autophagy, and epigenetic modifications. However, interleukin-27 can have the opposite effect and induce inflammation and cell death in certain situations. In this review, we describe the current understanding of regulatory activities of interleukin-27 on cell survival and inflammation and discuss its mechanisms of action in the brain, spinal cord, and retina. We also review evidence for and against the therapeutic potential of interleukin-27 for dampening harmful neuroinflammatory responses in central nervous system diseases. |
first_indexed | 2024-04-11T17:17:03Z |
format | Article |
id | doaj.art-8d16be875b084bb4aadc3d48cf1d0a71 |
institution | Directory Open Access Journal |
issn | 1673-5374 |
language | English |
last_indexed | 2024-04-11T17:17:03Z |
publishDate | 2022-01-01 |
publisher | Wolters Kluwer Medknow Publications |
record_format | Article |
series | Neural Regeneration Research |
spelling | doaj.art-8d16be875b084bb4aadc3d48cf1d0a712022-12-22T04:12:36ZengWolters Kluwer Medknow PublicationsNeural Regeneration Research1673-53742022-01-0117102149215210.4103/1673-5374.336134Exploring the role of interleukin-27 as a regulator of neuronal survival in central nervous system diseasesAndrea N NorteyKimberly N GarcesAbigail S HackamInterleukin-27 is a pleiotropic cytokine that is involved in tissue responses to infection, cell stress, neuronal disease, and tumors. Recent studies in various tissues indicate that interleukin-27 has complex activating and inhibitory properties in innate and acquired immunity. The availability of recombinant interleukin-27 protein and mice with genetic deletions of interleukin-27, its receptors and signaling mediators have helped define the role of interleukin-27 in neurodegenerative diseases. Interleukin-27 has been well-characterized as an important regulator of T cell activation and differentiation that enhances or suppresses T cell responses in autoimmune conditions in the central nervous system. Evidence is also accumulating that interleukin-27 has neuroprotective activities in the retina and brain. Interleukin-27 is secreted from and binds to infiltrating microglia, macrophage, astrocytes, and even neurons and it promotes neuronal survival by regulating pro- and anti-inflammatory cytokines, neuroinflammatory pathways, oxidative stress, apoptosis, autophagy, and epigenetic modifications. However, interleukin-27 can have the opposite effect and induce inflammation and cell death in certain situations. In this review, we describe the current understanding of regulatory activities of interleukin-27 on cell survival and inflammation and discuss its mechanisms of action in the brain, spinal cord, and retina. We also review evidence for and against the therapeutic potential of interleukin-27 for dampening harmful neuroinflammatory responses in central nervous system diseases.http://www.nrronline.org/article.asp?issn=1673-5374;year=2022;volume=17;issue=10;spage=2149;epage=2152;aulast=central nervous system; cytokine; inflammatory; interleukin-27; neuroprotection; retina |
spellingShingle | Andrea N Nortey Kimberly N Garces Abigail S Hackam Exploring the role of interleukin-27 as a regulator of neuronal survival in central nervous system diseases Neural Regeneration Research central nervous system; cytokine; inflammatory; interleukin-27; neuroprotection; retina |
title | Exploring the role of interleukin-27 as a regulator of neuronal survival in central nervous system diseases |
title_full | Exploring the role of interleukin-27 as a regulator of neuronal survival in central nervous system diseases |
title_fullStr | Exploring the role of interleukin-27 as a regulator of neuronal survival in central nervous system diseases |
title_full_unstemmed | Exploring the role of interleukin-27 as a regulator of neuronal survival in central nervous system diseases |
title_short | Exploring the role of interleukin-27 as a regulator of neuronal survival in central nervous system diseases |
title_sort | exploring the role of interleukin 27 as a regulator of neuronal survival in central nervous system diseases |
topic | central nervous system; cytokine; inflammatory; interleukin-27; neuroprotection; retina |
url | http://www.nrronline.org/article.asp?issn=1673-5374;year=2022;volume=17;issue=10;spage=2149;epage=2152;aulast= |
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