Alteration in murine epidermal Langerhans cell population by various UV irradiations: quantitative and morphologic studies on the effects of various wavelengths of monochromatic radiation on Ia-bearing cells.

The present study was undertaken in order to clarify the exact mode of the Langerhans cell (LC) depleting process caused by UV irradiation. Following irradiation with a single dose of various wavelengths of monochromatic UV radiation (UVR), we studied the number of Ia-positive cells in mouse epidermal sheets quantitatively, particularly with regard to dose-response relationship, action spectrum, and time course change. In addition, we studied morphologic alterations of these cells using electron- and immunoelectron microscopy (EM and IEM). We obtained the following results after a single dose of UVB radiation (200 mJ/cm2 of 300 nm) or PUVA (1% of 8-methoxypsoralen (8-MOP) 20 microliter and 1 J/cm2 of 360 nm): (1) EM and IEM showed that while some LCs simply lost their Ia marker without any structural alterations, the majority of the LCs disappeared due to actual cell damage. (2) During an "injury phase," the initial 48 h, and a "recovery phase," lasting from 4-14 days after irradiation, enlargement of the size of remaining Ia-positive LCs occurred. The degree of enlargement was closely related to the degree of reduction in number, suggesting a process compensating for the loss of the LC population. (3) It was found that the recovery rate of LCs after irradiation damage was slower than that of keratinocytes, indicating different cell kinetics between these distinct cell populations in the epidermis, i.e., restoration of LCs after irradiation seems to be achieved at least partially through a repopulation process originating in the bone marrow. Studies with irradiation of various monochromatic wavebands, with or without topical 8-MOP, showed that the action spectrum for Ia-positive cell depletion activity lay within the spectrum shorter than 300 nm for UVR alone, and between 320-380 nm for 8-MOP plus UVR. Since the action spectra were similar to those for keratinocyte damage, i.e., sunburn cell formation, induction of unscheduled DNA synthesis, and to those for UVR-induced erythema, we conclude that common mechanisms underlie these types of tissue damage.