Figure Supplementary 1: Skin TRM cells mediate local antiviral protection.
Frequency a and CD69 and CD103 expression b of CD45.1+ gBT-I T cells isolated from DNFB-treated skin (upper panel) or non-treated contralateral flank skin (lower panel). Data are representative of 2 experiments with n = 5 group. c Schematic depicting “patch” protection model. Mice were seeded with effector gBT-I cells and treated with DNFB on the lower left skin flank to lodge TRM cells. >30 d post DNFB treatment, mice were infected with HSV on the upper left skin flank so that infection could be initiated in the absence of TRM, leading to primary (1°) infection of the upper skin region and the dorsal root ganglion (DRG). Viral emergence from the DRG results in secondary (2°) lesion formation, which is interrupted in DNFB-treated skin patch containing TRM cells. d Photographs depicting 1° and 2° lesion formation in DNFB-treated skin possessing a “patch” of TRM cells on the lower left flank (DNFB + TRM, left panel) or on the non-treated contralateral flank (right panel) 6d after HSV infection. Data are representative of 2 experiments with n = 5 group.
