Effects of neurons and astrocytes on T lymphocyte activation

초록

After brain tissue damage occurred, various immune cells are introduced to cause neuro-inflammation. In this case, astrocytes protect neurons and interact with T cells to play an important role in brain inflammation. However, it is difficult to study how T cells interact with astrocytes or neurons in vivo due to restricted number of T cells in brain tissue. Therefore, we analyzed the phenotype of T cells and the level of cytokine expression through the in vitro co-culture system of lymphocytes either astrocytes or neurons. Astrocytes and neurons were obtained from neonatal mouse brain cortex and embryonal cortex, respectively. They were co-cultured with T cells activated by anti-CD3/CD28 antibodies. In the presence of astrocytes or neurons, the percentage of effector CD44 hi CD62L lo T cells were increased, while IL-4, IL-13, IL-17A, and IFN-γ cytokines were decreased in the culture medium. In contrast to the neurons, astrocytes induced IL-6 and produced nitric oxide (NO). Expression of IFN-γ was partially restored by NO inhibitor L-NMMA. Intriguingly, the expression of CD62L was fully restored by PI3 kinase inhibitor (Ly294002) or rapamycin. Based on these results, neurons and astrocytes can influence the intrinsic signals of T cells to maintain effector T cells which probably affect the brain inflammation. The detailed mechanisms of how astrocytes and neurons affect T cells need to be studied in the future.