In:
Journal of Cerebral Blood Flow & Metabolism, SAGE Publications, Vol. 42, No. 11 ( 2022-11), p. 2048-2057
Abstract:
Immunosuppression commonly occurs after a stroke, which is believed to be associated with the increased risk of infectious comorbidities of stroke patients, while the mechanisms underlying post-stroke immunosuppression is yet to be elucidated. In the brains of intracerebral hemorrhage (ICH) patients and murine ICH models, we identified that neuron-derived programmed death-ligand 1 (PD-L1) is reduced in the perihematomal area, associating increased soluble PD-L1 level in the peripheral blood. ICH induced a significant decrease of T and natural killer (NK) cell numbers in the periphery with an upregulation of programed death-1 (PD-1) in these cells. Blocking PD-1 pathway with an anti-PD1 monoclonal antibody prevented the T and NK cell compartment contraction and spleen atrophy post-ICH, with reduced pulmonary bacterial burden and improved neurological outcome. Thus, we here identified that brain-derived PD-L1 as a new mechanism driving post-stroke immunosuppression, and anti-PD1 treatment could be potentially developed to reducing the risk of post-stroke infections.
Type of Medium:
Online Resource
ISSN:
0271-678X
,
1559-7016
DOI:
10.1177/0271678X221116048
Language:
English
Publisher:
SAGE Publications
Publication Date:
2022
detail.hit.zdb_id:
2039456-1
