The presence of T regulatory cells (Tregs) in the skin is important to controlling inflammatory responses in this peripheral tissue. The dermis of uninflamed skin contains a population of relatively immotile Tregs often located in clusters around hair follicles. Inflammation induces a significant increase both in the abundance of Tregs within the dermis, and in the proportion of Tregs that are highly migratory. The molecular mechanisms underpinning alterations in Treg migration and retention in the dermis are unclear. To address this, we used multiphoton microscopy to examine Foxp3-GFP (Treg reporter) mice in order to investigate dermal Treg migration in the absence of inflammation, and during the peak (24 hours) and resolution (48 hours) phases of oxazolone-induced contact sensitivity (CS). These studies demonstrated that integrins play differential roles in Treg migration, varying according to the phase of the inflammatory response. Alphav integrin is important for Treg migration during the peak of inflammation but is dispensable at later time points, while AlphaE integrin has no functional contribution to Treg migration in uninflamed skin or at the peak of inflammation, but is important for Treg retention at later time points. Similarly, Beta1 integrin does not play a role in Treg migration during the peak of inflammation but is important for Treg retention at later time points. In contrast, inhibition of PI3K p110d signalling reduced Treg migration at all time points tested. Together these observations demonstrate that the molecular mechanisms controlling intradermal Treg migration vary markedly according to the phase of inflammatory response.