UVB exposure-induced systemic modulation of Th1-and Th2-mediated immune responses

Exposure to ultraviolet light, especially UVB wavelengths, can impair immun e responses in animals and humans. It is remarkable that this immunomodulat ion is not restricted to the exposed skin but is also found at other sites, i.e. systemic (distant) immunosuppression. A frequently proposed hypothesi s is that UVB exposure inhibits, specifically, T helper 1 (Th1)-mediated im mune responses. The major reason for this is that contact hypersensitivity (CHS) and delayed-type hypersensitivity (DTH), both Th1-mediated immune res ponses, are very sensitive to UVB. For this reason these models are frequen tly used for photoimmunology studies. In the present study, the effects of UVB exposure were investigated in classical models for Th1-mediated immunit y, i.e. CHS models in which picrylchloride or oxazolone were used as low-mo lecular-weight chemical antigens. In these models, CHS responsiveness and c ytokines were-measured, the latter by both reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). The CHS responses to both contact sensitizers (picrylchloride and oxazolone) w ere suppressed significantly by pre-exposure to repeated suberythemal UVB e xposure. Interferon-gamma (IFN-gamma), interleukin (IL)-12 and IL-4, but no t IL-10, were detectable in spleen and draining lymph nodes of sensitized B ALB/c mice. Repeated UVB exposure prior to sensitization at a distant locus inhibited both IFN-gamma and IL-12 but not IL-4. In BALB/c mice sensitized with ovalbumin (OVA) in the absence of complete Freund's adjuvant,a model for Th2-mediated immunity, OVA-specific serum IgE and cytokine profiles in the spleen were analysed. Sensitization did lead to a significant increase in OVA-specific IgE serum titres. Pre-exposure to UVB resulted in a decreas ed OVA-specific IgE serum titre. Both RT-PCR and ELISA showed increased lev els of IFN-gamma, IL-4 and IL-10 in the spleens of OVA-sensitized mice. The production of IFN-gamma and IL-4 was not affected by UVB pre-exposure. In contrast, the production of IL-10 was significantly increased. This was pro bably caused by an up-regulation of Th2 cells. It is remarkable that IFN-ga mma is significantly suppressed by UVB in Th1-mediated immune reactions but not in Th2-mediated immune reactions where it even appears to increase. IL -10, which is up-regulated by UVB pre-exposure and produced by, among other s, Th2 cells, may represent a shift from Th1- to Th2-mediated immune mechan isms. However, IL-10 can also inhibit Th2 responses, which might be the rea son for a decreased IgE titre in the Th2 model. From the results of this st udy it is concluded that UVB exposure prior to sensitization/immunization n ot only inhibits Th1-mediated but also Th2-mediated immune responses.