The activation of CD4 T cells is accompanied by functional specialization which allows for the development of pathogen specific responses with appropriate effector responses as well as the imprinting of tissue homing signals that facilitates the recruitment of effector T cells to sites of infection. However, the extent to which T helper (Th) differentiation is coordinately regulated with the expression of tissue-specific homing receptors is unclear. To better define this relationship, HSV-1-specific CD4 T cells (gDT-II cells) were adoptively transferred into C57BL/6 mice which were then infected with HSV. Infection of the flank induced the expression of E-Selectin Ligand (ESL), a carbohydrate modification required for skin homing. In contrast, gDT-II cells recovered following intranasal infection lacked ESL. Flank infection directed a Th1 response with the majority of gDT-II cells expressed Tbet. Comparison of the kinetics of Tbet and ESL expression showed that the induction of Tbet expression preceded that of ESL which was only observed in cells that had undergone multiple rounds of division. To determine whether Th1-promoting cytokines have a role in regulating ESL, we adoptively transferred gDT-II cells to IL-12-, IFNg-, or IL-18-deficient mice, and following skin infection found a similar proportion of ESL⁺ gDT-II cells to wild-type mice. However, there were no significant differences in the proportion of Tbet⁺ cells, suggesting a degree of redundancy in the factors that drive Th1 differentiation in this model. Consequently we assessed the induction of ESL expression on Tbet-deficient gDT-II cells. Following skin infection, gDT-II cells acquired Th17 phenotype, expressing RORgT and producing IL-17. Nevertheless, there was no difference in the proportion of gDT-II cells that expressed ESL. Thus the induction of the tissue-specific homing receptor ESL is not strictly linked with Th1 differentiation but rather allows for cells with distinct functional capacities to be recruited to the skin.