Infection triggers large-scale changes in the phenotype and function of CD8+T cells that are critical for immune clearance and the formation of immunological memory, however, the gene regulatory mechanisms that control these changes are largely unknown. Posttranslational modification of histone proteins regulate gene transcription by either directly affecting chromatin compaction, or by serving as substrates for binding of chromatin remodeling complexes that influence gene regulation by various mechanisms. Polycomb Repressive complexes (PRC) are chromatin remodeling complexes implicated in silencing genes encoding crucial developmental regulators, which have functions in the context of embryonic stem cell differentiation, maintenance of pluripotency and lineage specification. PRCs can be grouped into two major types: PRC1 and PRC2. PRC2 acts upstream and catalyzes the trimethylation of lysine 27 of Histone 3 which is read by PRC1 and in turn PRC1 monoubiquitinates the lysine 119 of Histone 2A leading to the chromatin compaction and transcriptional silencing. However, it is not clear whether these findings extend beyond stem cell biology and represent a general mechanism by which cellular differentiation is regulated. We hypothesize that regulated expression of components of the PRC1 complex modulates the CD8+ T cell differentiation. In our study we are exploring the role of CBX4, CBX7, and BMI1 – components of PRC1 – in the context of virus-driven CD8+T cell differentiation. Our data show that the expression of these genes is highly regulated through the different phases of CD8+T cell differentiation. Moreover, TCR signaling plays a crucial role in their expression, with the strength and affinity of TCR stimulation modulating the transcription of all three genes. Taken together, our data suggest that a role for PRC1 in regulating CD8+T cell differentiation.