Akademik Veri Yönetim Sistemi
European Human Genetics Conference, Berlin, Almanya, 1 - 04 Haziran 2024
BACKGROUND: Microglial cells which are brain-resident immune cells are responsible for
innate immunity and have vital importance initiation of neuroimmune responses to various
conditions such as brain injury, infection and neurodegeneration. The programmed death (PD)-
1/PD-L1 pathway results in functional inhibition of T cells and it is a known negative immune
checkpoint. PD-1/PD-L1 pathway reduces excessive immune reaction and prevents cellular
toxicity. In this study, we aimed to investigate changes in expression of PD-1 and PD-L1 genes
after activation of N9 microglial cells with Lipopolysaccharide.
METHODS: N9 microglial cells were treated with 100 ng/mL LPS for 24 hours. After RNA
isolation and cDNA synthesis, Real-time PCR reactions were performed for PD-1 and PD-L1
genes. Relative mRNA levels of the genes was calculated by 2-ΔΔCt method. Independent
samples t-test was used to compaire differences in expression levels of the genes between
control and LPS-treated cells.
RESULTS: In this study, we determined that the expression level of PD-L1 gene was
significantly increased in N9 microglial cells that were treated with 100 ng/mL LPS. However,
we did not find any statistically differences in expression level of PD-1 gene between control
and LPS-treated cells.
CONCLUSION: In this study, we showed that PD-L1 expression was increased in LPSactivated microglia cells. Therefore our results suggest that PD-1/PD-L1 pathway, a negative
immune regulatory system of T cells, can play an important role in LPS-induced
neuroinflammation.
Grant: This work was supported by “Cukurova University Research Projects Funding Unit” with
project number:TSA-2022-14801.