Modulation of Neuroinflammation: Advances in Roles and Mechanisms of the IL-33/ST2 Axis Involved in Ischemic Stroke.
Neuroimmunomodulation
; 30(1): 226-236, 2023.
Article
en En
| MEDLINE
| ID: mdl-37729881
ABSTRACT
Interleukin (IL)-33 was initially recognized as a constituent of the IL-1 cytokine family in 2005. It exerts pleiotropic effects by regulating immune responses via its binding to the receptor ST2 (IL-33R). The IL-33/ST2 pathway has been linked to several inflammatory disorders. In human and rodents, the broad expression of IL-33 in spinal cord tissues and brain indicates its central nervous system-specific functions. Growing evidence supports the protective effects of the IL-33/ST2 pathway in ischemic stroke, along with a better understanding of the underlying mechanisms. IL-33 plays a crucial role in the regulation of the release of inflammatory molecules from glial cells in response to neuropathological lesions. Moreover, IL-33/ST2-mediated neuroprotection following cerebral ischemia may be linked to T-cell function, specifically regulatory T cells. Soluble ST2 (sST2) acts as a decoy receptor in the IL-33/ST2 axis, blocking IL-33 signaling through the membrane ST2 receptor. sST2 has also been identified as a potential inflammatory biomarker of ischemic stroke. Targeting sST2 specifically to eliminate its inhibition of the protective IL-33/ST2 pathway in ischemic brain tissues is a promising approach for the treatment of ischemic stroke.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Isquemia Encefálica
/
Interleucina-33
/
Proteína 1 Similar al Receptor de Interleucina-1
/
Accidente Cerebrovascular Isquémico
Límite:
Humans
Idioma:
En
Revista:
Neuroimmunomodulation
Asunto de la revista:
ALERGIA E IMUNOLOGIA
/
NEUROLOGIA
Año:
2023
Tipo del documento:
Article
País de afiliación:
China