Interferon beta modulates major histocompatibility complex class I (MHC I) and CD3-zeta expression in PC12 cells

It has been demonstrated that the major histocompatibility complex of class I (MHC I) up regulation by exogenous treatment with interferon beta (IFNbeta) influences the glial reaction and synaptic elimination process. Therefore, the present study aimed to investigate the effects of IFNbeta treatment on the expression of MHC I, CD3-zeta (a subunit of MHC I receptor) and synaptic formation in PC12 cells, an in vitro model for studying the synaptic formation/elimination process. For this purpose, established cultures were subjected to IFNbeta (500 and 1000 IU/ml) treatment for 5, 10 and 15 days. The cells were then fixed and processed for immunocytochemistry with antisera against MHC I (OX18), CD3-zeta and synaptophysin. The results were compared with control cultures only treated with basal medium. IFNbeta (500 IU/ml) modulated the MHC I expression in PC12 cells, especially after 10 days of treatment. In this sense, IFNbeta induced MHC I as well as CD3-zeta up regulation. It was observed that the highest dose caused culture degeneration. Interestingly, differential regulation of MHC I was paralleled by enhancement in synaptic network remodeling. Altogether, the present data indicate that PC12 cells may be used as an in vitro model for studying MHC I modulation and synaptic plasticity. It also reinforced the role of IFNbeta on the synaptic elimination process.

► PC12 cells may be considered as an alternative model to studying MHC I regulation and synaptic plasticity.
► Synapse formation in PC12 cells is affected by MHC I upregulation in response to IFNbeta treatment.
► PC12 cells express CD3-zeta, a subunit of TCR that is fundamental for post synaptic MHC I signal transduction.