Role of dermal cells from normal and ultraviolet B-damaged skin in induction of contact hypersensitivity and tolerance. 
With conventional regimens for induction of contact hypersensitivity with highly reactive haptens, circumstantial evidence implicates both epidermal and dermal APC.  However, similar applications of hapten to skin that has been treated with an acute, low dose UVB radiation protocol induce contact hypersensitivity only in certain genetically defined strains of mice, termed UVB-resistant.  Moreover, mice that fail to acquire contact hypersensitivity when hapten is painted on UVB-exposed skin display hapten-specific tolerance.  In the present study, dermal cell suspensions have been prepared from normal and UVB-exposed mouse skin as a means of identifying the cell(s) that: 1) provide APC function after UVB radiation in UVB-resistant mice; and 2) confer tolerance after UVB radiation in UVB-susceptible mice.  The results confirm that the normal murine dermis contains Ia+ cells that, when hapten-derivatized in vitro and injected s.c.  into naive, syngeneic mice, possess typical Ag-presenting function.  Cells with similar function are retained in the dermis of UVB-resistant mice after exposure to UVB radiation, whereas dermal cells of UVB-exposed skin of UVB-susceptible mice display no ability to induce contact hypersensitivity.  Instead, the latter dermal cells, when hapten-conjugated and injected s.c.,  induce tolerance.  Thus, doses of UVB radiation that deplete the epidermis of Langerhans cells do not deplete the dermis of UVB-resistant mice of contact hypersensitivity-inducing APC, but do confer upon cells within the dermis of UVB-susceptible mice the capacity to induce unresponsiveness.