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Splenic contribution to the recovery of ATPase/Ia+ epidermal cells in the skin of mice after exposure to ultraviolet radiation.

The density of Langerhans cells (LC) is significantly decreased in skin sites exposed to ultraviolet radiation (UVR). This results in reduced antigen-presenting cell (APC) activity in UVR-exposed skin. We have previously reported that the recovery in the density of ATPase/Ia+ epidermal cells (EC) parallels the restoration of APC function in the UVR-exposed skin of mice. The present study was designed to determine whether the spleen might serve as a source of ATPase/Ia+ cells to restore APC function to the skin after UVR exposure. ATPase/Ia+ EC densities were calculated from skin biopsies taken from BALB/c mice at various time points after low dose UVR treatment (2000 J/m2 protracted over 4 days). The recovery rate of ATPase/Ia+ EC in splenectomized mice after UVR exposure was similar, although delayed, compared to that of sham-operated mice. For example, 3 days after UVR exposure the density of ATPase/Ia+ EC in sham controls was 90% of normal and exceeded normal values by 5 days. In contrast, ATPase/Ia+ EC density in splenectomized mice was 60% of normal at 3 days and did not exceed normal values until 7 days after UVR exposure. Normal recovery of ATPase/Ia+ EC was restored to splenectomized mice given an adoptive transfer of syngeneic spleen cells immediately after UVR exposure. Fluorescein-labeled spleen cells used for adoptive transfer were observed within the epidermis of splenectomized mice 1 and 3 days after UVR exposure. Indirect immunofluorescent staining employing phycoerythrin-labeled reagents revealed that the fluorescein-labeled splenic EC expressed Ia, MAC-1, CLA, and Fc-receptor molecules. These results indicate that a portion of the ATPase/Ia+ EC that recovery after UVR exposure originate from the spleen. These cells may be distinct from LC, but appear to restore APC function to the skin following LC depletion by UVR exposure.