CXCR3-mediated natural killer cell infiltration exacerbates white matter injury after intracerebral haemorrhage.

ABSTRACT: Intracerebral haemorrhage (ICH), a subtype of stroke, carries a grim prognosis. The inflammatory response during the early phase of ICH is a major perpetuator of neurological damage. Recent clinical studies suggest possible participation of the CXC chemokine receptor 3 (CXCR3)-chemokine system in mediating neuroimmune crosstalk, which exacerbates neurological dysfunction and might serve as a potential therapeutic target in the management of ICH. CXCR3 is expressed by natural killer (NK) cells, which are known to be pathogenic in ICH. However, whether and how CXCR3 promotes NK cell infiltration and functioning in ICH and whether the attenuation of CXCR3 might affect neurological outcome have not been delineated. The present preclinical study has demonstrated, for the first time, the role of

SUBMITTER: Ng ACK 

PROVIDER: S-EPMC12404770 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature