Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2025 Jan;62(1):518-532.
doi: 10.1007/s12035-024-04281-7. Epub 2024 Jun 14.

Role of Regulatory T Cells in Intracerebral Hemorrhage

Yaxin Shang  1 , Lei Zheng  2   3 , Yunpeng Du  1 , Tong Shang  1 , Xueting Liu  1 , Wei Zou  4   5
Affiliations
Review

Role of Regulatory T Cells in Intracerebral Hemorrhage

Yaxin Shang et al. Mol Neurobiol. 2025 Jan.

Abstract

Intracerebral hemorrhage (ICH) is a common cerebrovascular disease that can lead to severe neurological dysfunction in surviving patients, resulting in a heavy burden on patients and their families. When ICH occurs, the blood‒brain barrier is disrupted, thereby promoting immune cell migration into damaged brain tissue. As important immunosuppressive T cells, regulatory T (Treg) cells are involved in the maintenance of immune homeostasis and the suppression of immune responses after ICH. Treg cells mitigate brain tissue damage after ICH in a variety of ways, such as inhibiting the neuroinflammatory response, protecting against blood‒brain barrier damage, reducing oxidative stress damage and promoting nerve repair. In this review, we discuss the changes in Treg cells in ICH clinical patients and experimental animals, the mechanisms by which Treg cells regulate ICH and treatments targeting Treg cells in ICH, aiming to support new therapeutic strategies for clinical treatment.

Keywords: Blood–brain barrier damage; Intracerebral hemorrhage; Nerve repair; Neuroinflammation; Oxidative stress; Regulatory T cells.

PubMed Disclaimer

Conflict of interest statement

Declarations. Ethics Approval: Not applicable. Consent to Participate: Not applicable. Consent for Publication: All authors read and approved the fnal manuscript. Competing Interests: The authors declare no competing interests.

Similar articles

See all similar articles

Cited by

References

    1. GBD 2019 Stroke Collaborators (2021) Global, regional, and national burden of stroke and its risk factors, 1990-2019: a systematic analysis for the Global Burden of Disease Study 2019. Lancet Neurol 20(10):795–820. https://doi.org/10.1016/s1474-4422(21)00252-0
    1. Keep RF, Hua Y, Xi G (2012) Intracerebral haemorrhage: mechanisms of injury and therapeutic targets. Lancet Neurol 11:720–731. https://doi.org/10.1016/s1474-4422(12)70104-7 - DOI - PubMed
    1. Jiang C, Guo H, Zhang Z, Wang Y, Liu S, Lai J, Wang TJ et al (2022) Molecular, Pathological, Clinical, and Therapeutic Aspects of Perihematomal Edema in Different Stages of Intracerebral Hemorrhage. Oxid Med Cell Longev 2022:3948921. https://doi.org/10.1155/2022/3948921 - DOI - PubMed - PMC
    1. Han X, Li Q, Lan X, El-Mufti L, Ren H, Wang J (2019) Microglial Depletion with Clodronate Liposomes Increases Proinflammatory Cytokine Levels, Induces Astrocyte Activation, and Damages Blood Vessel Integrity. Mol Neurobiol 56:6184–6196. https://doi.org/10.1007/s12035-019-1502-9 - DOI - PubMed - PMC
    1. Askenase MH, Sansing LH (2016) Stages of the Inflammatory Response in Pathology and Tissue Repair after Intracerebral Hemorrhage. Semin Neurol 36:288–297. https://doi.org/10.1055/s-0036-1582132 - DOI - PubMed - PMC

MeSH terms

LinkOut - more resources