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Cells
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Stroke Immunology: Mechanisms and Therapeutic Prospects
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Stroke Immunology: Mechanisms and Therapeutic Prospects

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: closed (31 March 2025) | Viewed by 9904

Special Issue Editors

Dr. Emmanuel Pinteaux

E-Mail Website
Guest Editor
FBMH, Division of Neuroscience, The University of Manchester, Manchester, UK
Interests: cerebrovascular disease; stroke; neuroinflammation; neurorepair
Dr. Alba Grayston-Morales

E-Mail Website
Guest Editor
Brain Inflammation Group, University of Manchester, Manchester, UK
Interests: stroke; neuroinflammation; neurorepair; preclinical stroke models

Special Issue Information

Dear Colleagues,

Stroke is a major cause of death and disability worldwide. Despite great advances in acute management due to improved recanalization strategies, greater symptom awareness and prompt intervention, the recanalization eligibility is still limited, and a large proportion of stroke patients remain disabled or die. Translational stroke research has focused on neuroprotection as a promising strategy alongside recanalization to limit tissue injury. However, out of more than 1000 putative neuroprotectants, none have reached the clinical setting and, with neurorehabilitation being the only available treatment beyond the acute phase, there is a flagrant need to enhance post-stroke recovery.

In recent years, stroke immunology has emerged as a promising field, placing emphasis on the inflammatory response as a key pathophysiological event contributing to tissue injury and repair. It is now known that stroke not only triggers a local neuroinflammatory response but also induces disturbances in systemic immune homeostasis, and common stroke risk factors are associated with inflammatory processes.

This Special Issue aims to provide mechanistic insights into the high complexity of local and systemic immune disturbances affecting the stroke pathogenesis and outcome and cover recent therapeutic advances targeting immune pathways after stroke. Authors are welcome to submit original research articles or topic reviews that expand our knowledge of stroke immunology.

Dr. Emmanuel Pinteaux
Dr. Alba Grayston-Morales
Guest Editors

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • stroke
  • neuroimmunology
  • neuroinflammation
  • thromboinflammation
  • blood-brain barrier
  • glia
  • immunomodulation

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Published Papers (3 papers)

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Review

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23 pages, 2242 KB  
Review
The Complex Role of the Complement C3a Receptor (C3aR) in Cerebral Injury and Recovery Following Ischemic Stroke
by Naseem Akhter, Ateeq Lambay, Reema Almotairi, Abdullah Hamadi, Kanchan Bhatia, Saif Ahmad and Andrew F. Ducruet
Cells 2025, 14(18), 1440; https://doi.org/10.3390/cells14181440 - 15 Sep 2025
Viewed by 917
Abstract
The Complement C3a Receptor (C3aR) plays a multifaceted role along the varying temporal phases of brain injury following cerebral ischemia. C3aR is a G-protein-coupled receptor (GPCR) that binds to its ligand, C3a an anaphylatoxin generated during activation of the complement cascade. During ischemia, [...] Read more.
The Complement C3a Receptor (C3aR) plays a multifaceted role along the varying temporal phases of brain injury following cerebral ischemia. C3aR is a G-protein-coupled receptor (GPCR) that binds to its ligand, C3a an anaphylatoxin generated during activation of the complement cascade. During ischemia, complement is activated as part of the initial inflammatory response, with C3aRs playing a time-dependent role in both brain injury and repair mechanisms. In the acute phase (minutes to hours post-ischemia), C3aR activation promotes the recruitment of immune cells and the release of chemokines and cytokines, driving blood–brain barrier (BBB) permeability and brain edema. During the subacute phase (hours to days post-ischemia), C3aR continues to modulate immune cell activity, worsening secondary brain injury, although emerging evidence suggests that C3aR activation in this phase may also aid in the clearance of cellular debris and cell survival. In the chronic phase (days to weeks post-ischemia), chronically elevated C3aR activity can prolong neuroinflammation and impair recovery, whereas controlled C3aR signaling in the subacute/chronic phase can activate reparative pathways (e.g., microglial phagocytosis, astrocyte trophic support). As a result, targeting the C3aR requires careful timing to optimize its benefits. Given the dual impact of C3aR activation, which serves to exacerbate injury in the acute phase but supports repair beginning in the subacute and chronic phases, a targeted therapeutic approach should focus on context- and time-dependent modulation of the C3a/C3aR axis. This strategy would involve blocking the C3aR during the acute phase to reduce inflammation and BBB breakdown while controlling C3a signaling in later phases to promote tissue repair. Full article
(This article belongs to the Special Issue Stroke Immunology: Mechanisms and Therapeutic Prospects)
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20 pages, 1296 KB  
Review
Exposure to Environmental Toxins: Potential Implications for Stroke Risk via the Gut– and Lung–Brain Axis
by Alexandria Ruggles and Corinne Benakis
Cells 2024, 13(10), 803; https://doi.org/10.3390/cells13100803 - 8 May 2024
Cited by 9 | Viewed by 5514
Abstract
Recent evidence indicates that exposure to environmental toxins, both short-term and long-term, can increase the risk of developing neurological disorders, including neurodegenerative diseases (i.e., Alzheimer’s disease and other dementias) and acute brain injury (i.e., stroke). For stroke, the latest systematic analysis revealed that [...] Read more.
Recent evidence indicates that exposure to environmental toxins, both short-term and long-term, can increase the risk of developing neurological disorders, including neurodegenerative diseases (i.e., Alzheimer’s disease and other dementias) and acute brain injury (i.e., stroke). For stroke, the latest systematic analysis revealed that exposure to ambient particulate matter is the second most frequent stroke risk after high blood pressure. However, preclinical and clinical stroke investigations on the deleterious consequences of environmental pollutants are scarce. This review examines recent evidence of how environmental toxins, absorbed along the digestive tract or inhaled through the lungs, affect the host cellular response. We particularly address the consequences of environmental toxins on the immune response and the microbiome at the gut and lung barrier sites. Additionally, this review highlights findings showing the potential contribution of environmental toxins to an increased risk of stroke. A better understanding of the biological mechanisms underlying exposure to environmental toxins has the potential to mitigate stroke risk and other neurological disorders. Full article
(This article belongs to the Special Issue Stroke Immunology: Mechanisms and Therapeutic Prospects)
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Other

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16 pages, 3155 KB  
Brief Report
GPR55 Inactivation Diminishes Splenic Responses and Improves Neurological Outcomes in the Mouse Ischemia/Reperfusion Stroke Model
by Sachin Gajghate, Hongbo Li and Slava Rom
Cells 2024, 13(3), 280; https://doi.org/10.3390/cells13030280 - 3 Feb 2024
Cited by 3 | Viewed by 2540
Abstract
Although strokes are frequent and severe, treatment options are scarce. Plasminogen activators, the only FDA-approved agents for clot treatment (tissue plasminogen activators (tPAs)), are used in a limited patient group. Moreover, there are few approaches for handling the brain’s inflammatory reactions to a [...] Read more.
Although strokes are frequent and severe, treatment options are scarce. Plasminogen activators, the only FDA-approved agents for clot treatment (tissue plasminogen activators (tPAs)), are used in a limited patient group. Moreover, there are few approaches for handling the brain’s inflammatory reactions to a stroke. The orphan G protein-coupled receptor 55 (GPR55)’s connection to inflammatory processes has been recently reported; however, its role in stroke remains to be discovered. Post-stroke neuroinflammation involves the central nervous system (CNS)’s resident microglia activation and the infiltration of leukocytes from circulation into the brain. Additionally, splenic responses have been shown to be detrimental to stroke recovery. While lymphocytes enter the brain in small numbers, they regularly emerge as a very influential leukocyte subset that causes secondary inflammatory cerebral damage. However, an understanding of how this limited lymphocyte presence profoundly impacts stroke outcomes remains largely unclear. In this study, a mouse model for transient middle cerebral artery occlusion (tMCAO) was used to mimic ischemia followed by a reperfusion (IS/R) stroke. GPR55 inactivation, with a potent GPR55-specific antagonist, ML-193, starting 6 h after tMCAO or the absence of the GPR55 in mice (GPR55 knock out (GPR55ko)) resulted in a reduced infarction volume, improved neurological outcomes, and decreased splenic responses. The inhibition of GPR55 with ML-193 diminished CD4+T-cell spleen egress and attenuated CD4+T-cell brain infiltration. Additionally, ML-193 treatment resulted in an augmented number of regulatory T cells (Tregs) in the brain post-tMCAO. Our report offers documentation and the functional evaluation of GPR55 in the brain–spleen axis and lays the foundation for refining therapeutics for patients after ischemic attacks. Full article
(This article belongs to the Special Issue Stroke Immunology: Mechanisms and Therapeutic Prospects)
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