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Published on: August 22, 2011
PD-L1 (Programmed Death Ligand 1) Protects Against Experimental Intracerebral Hemorrhage-Induced Brain Injury
Ranran Han1, Jiaying Luo1, Yanchao Shi1
1From the Department of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, China.
Insights
Programmed death ligand 1 (PD-L1) shows therapeutic potential for intracerebral hemorrhage (ICH), a severe stroke. PD-L1 treatment reduced brain damage and improved neurological function in a preclinical ICH model.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Intracerebral hemorrhage (ICH) is a devastating stroke with no effective treatments.
- Current research explores novel therapeutic targets for ICH management.
Purpose of the Study:
- To investigate the therapeutic efficacy of programmed death ligand 1 (PD-L1) in a preclinical model of ICH.
- To elucidate the underlying mechanisms of PD-L1's action in the context of ICH.
Main Methods:
- An ICH mouse model was established by injecting autologous blood.
- Mice received intraperitoneal injections of vehicle, PD-L1, or anti-PD-L1 antibody.
- Evaluated neurological function, brain edema, immune cell infiltration, blood-brain barrier integrity, neuronal death, and mTOR pathway activity.
Main Results:
- PD-L1 treatment significantly improved neurological deficits, reduced brain edema, and decreased hemorrhage volume.
- PD-L1 modulated T cell populations in the brain, shifting towards regulatory and Th2 cells while decreasing Th1 and Th17 cells.
- Observed enhanced blood-brain barrier integrity, reduced neuronal death, and inhibition of the mTOR pathway with PD-L1 treatment.
Conclusions:
- PD-L1 demonstrates protective effects against the damaging consequences of intracerebral hemorrhage.
- PD-L1 represents a promising therapeutic candidate for treating ICH.
Background And Purpose:
Intracerebral hemorrhage (ICH) is a neurologically destructive stroke, for which no valid treatment is available. This preclinical study examined the therapeutic effect of PD-L1 (programmed death ligand 1), a B7 family member and a ligand for both PD-1 (programmed death 1) and B7-1 (CD80), in a murine ICH model.
Methods:
ICH was induced by injecting autologous blood into 252 male C57BL/6 and Rag1-/- mice. One hour later, ICH mice were randomly assigned to receive an intraperitoneal injection of vehicle, PD-L1, or anti-PD-L1 antibody. Neurological function was assessed along with brain edema, brain infiltration of immune cells, blood-brain barrier integrity, neuron death, and mTOR (mammalian target of rapamycin) pathway products.
Results:
PD-L1 significantly attenuated neurological deficits, reduced brain edema, and decreased hemorrhage volume in ICH mice. PD-L1 specifically downsized the number of brain-infiltrating CD4+ T cells and the percentages of Th1 and Th17 cells but increased the percentages of Th2 and regulatory T cells. In the PD-L1-treated group, we observed an amelioration of the inflammatory milieu, decreased cell death, and enhanced blood-brain barrier integrity. PD-L1 also inhibited the mTOR pathway. The administration of anti-PD-L1 antibody produced the opposite effects to those of PD-L1 in ICH mice.
Conclusions:
PD-L1 provided protection from the damaging consequences of ICH.
