AI Article Synopsis
- The study compares the effects of free alpha-galactosylceramide (αGalCer) and αGalCer-loaded dendritic cells (DCG) on liver injury in mice.
- While both treatments activate invariant natural killer T (iNKT) cells, only αGalCer caused significant liver injury, particularly in CD31-positive endothelial cells.
- DCG led to increased serum alanine transaminase (ALT) levels but did not result in lethal injury, suggesting different mechanisms of action and safety profiles between the two methods.
Article Abstract
Background/aim: Both free alpha-galactosylceramide (αGalCer) and αGalCer-loaded dendritic cells (DCG) activate invariant natural killer T (iNKT) cells to varying degrees, with αGalCer inducing liver injury. We sought to evaluate liver injury by these two pathways.
Materials And Methods: Mice were injected with αGalCer or DCG followed by analysis of serum alanine transaminase (ALT) activity levels, mortality and liver function.
Results: While ALT levels were elevated after DCG in a tumor necrosis factor (TNF)-α-dependent manner, DCG did not cause lethal injury. More serious injury of liver CD31-positive endothelial cells (CD31(+) EC) was observed in mice treated with αGalCer than with DCG. Furthermore, liver CD31(+) EC of αGalCer-treated mice induced naïve liver lymphocytes to produce TNF-α.
Conclusion: DCG treatment did not induce lethal liver injury. CD31(+) EC may play an antigen-presenting role to iNKT cells after αGalCer treatment and may be a cause of lethal injury.
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