We performed a time course study in order to define the in vivo relationship between the induction of active suppression of contact sensitization and the presence of various cells in ultraviolet-exposed dermis and epidermis implicated in locally inducible immune tolerance: class II major histocompatibility complex (MHC)(+)CD11b(lo)Gr-1(-) Langerhans cells (LC), class II MHC(-)CD45(+)CD3(+) dendritic epidermal T cells, class II MHC(+)CD11b(+)Gr-1(-) monocytes or class II MHC(+)CD11b(+)Gr-1(+) monocytic/macrophagic cells, Partial tolerance (50%) was first detectable 6 h after a single 72 mJ/cm(2) ultraviolet B exposure and maximum tolerance at 48 h post-ultraviolet exposure, By how cytometry, a low granularity LC subset had disappeared from the epidermis within 6 h after ultraviolet exposure, followed by a slower decrease in the high granularity Langerhans cells subset, Within the dermis at the 6-h time point, small numbers of infiltrating monocytic/macrophagic cells are already apparent, By 24 h post-ultraviolet exposure, at which time tolerance has increased to 70%, the infiltrating monocytic/macrophagic population had risen to 1.2% of the total dermal cell population and was observed for the first time in the epidermis along with other infiltrating leukocytes (i.e., polymorphonuclear leukocytes), By 48 h post-ultraviolet exposure, when a state of maximum tolerance is obtained, both constitutive epidermal and dermal antigen-presenting cell populations were at or near their nadir of depletion, The infiltrating monocyte/macrophage population, however, exhibited a dramatic increase in the epidermis at 48 and 72 h, Thus, the ability to locally induce a state of in vivo tolerance is closely associated with the expansion of class II MHC(+)CD11b(+)Gr-1(+) and monocytic/macrophagic cells in the dermis and epidermis.