Differential effects of UVA1 and UVB radiation on Langerhans cell migration in mice

The WE (280-315 nm)- and UVA1 (340-400 nm)-induced migration of Langerhans cells (LC) from the epidermis and accumulation of dendritic cells (DC) in t he lymph nodes draining the exposed skin site of C3H/HeN mice have been inv estigated. One minimum erythemal dose (MED) of UVB (1.5 kJ/m(2)) and of UVA 1 (500 kJ/m(2)) were chosen, which have been shown previously to suppress d elayed hypersensitivity (DTH). UVB irradiation resulted in a reduction in e pidermal LC numbers, local to the site of the exposure, which was most appa rent 12 h after exposure, but, in contrast, UVA1 had no significant effect even at 72 h after exposure. UVA1 did not exert any protection against the UVB-mediated depletion in LC numbers. The reduction in local LC following U VB exposure was prevented by systemic (intraperitoneal) treatment of mice w ith neutralising antibodies to either tumor necrosis factor (TNF)-alpha or interleukin (IL)-beta 2 h prior to the irradiation. It has been reported pr eviously that UVB exposure caused an increase in the number of dendritic ce lls (DC) in the lymph nodes draining the irradiated skin site. In the prese nt study we have shown that UVA1 had a similar effect. Pretreatment of the mice with neutralising antibodies to IL-1 beta (by intraperitoneal injectio n) substantially inhibited DC accumulation induced by both UV regimens. How ever, anti-TNF-alpha antibodies affected only the UVB-induced increase, and did not alter the elevation in DC numbers observed following UVA1 exposure . These results indicate that UVB causes the migration of LC from the epide rmis and an accumulation of DC in the draining lymph nodes by a mechanism t hat requires both TNF-alpha and IL-1 beta. In contrast, UVA1 does not cause LC migration from the epidermis and the accumulation of DC in the draining lymph nodes observed following UVA1 exposure requires IL-1 beta, but not T NF-alpha. It is likely therefore that UVA1 acts through a different mechani sm from UVB and may target a cutaneous antigen presenting cell other than L C, such as the dermal DC. (C) 2000 Elsevier Science S.A. All rights reserve d.