The heterodimeric integrin receptor Î±VÎ²8 is expressed by both CD103+ dendritic cells (DCs) and regulatory T-cells (Tregs). Its main function is to activate the latent form of the anti-inflammatory cytokine Transforming Growth Factor Î² (TGFÎ²) via the removal of the Latency Associated Peptide (LAP). Loss of Î±VÎ²8 integrin on murine DCs results in age-related autoimmunity and spontaneous development of colitis. Loss of Î±VÎ²8 integrin on Tregs attenuated their ability to suppress effector T-cell responses during ongoing inflammation. Integrins initiate intracellular signalling cascades following binding of their ligand, yet little is known about the intracellular effects of Î±VÎ²8 integrin ligation and how this may contribute to its role in immune regulation. We aimed to use RNA-sequencing analysis to elucidate potential novel Î±VÎ²8 mediated transcriptional changes within primary murine DCs and Tregs after incubation with LAP. We found that LAP incubation resulted in the significant upregulation and downregulation of 41 protein-coding genes in DCs and 164 protein-coding genes in Tregs. Importantly, these genes were not significantly altered in DCs or Tregs lacking the Î±VÎ²8 integrin and may therefore be altered due to LAP-Î±VÎ²8-mediated signalling. We also found that over a quarter of the total genes in DCs lacking Î±VÎ²8 integrin were significantly altered compared to wild-type (WT) DCs, whereas 199 genes in Tregs lacking Î±VÎ²8 integrin were significantly altered compared to WT Tregs. These data can be used as a platform upon which to base further experiments to identify potential novel functional mechanisms of Î±VÎ²8 integrin, enabling the identification of potential therapeutic targets to restore and promote immune tolerance via the Î±VÎ²8-TGFÎ² pathway.