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Department of Immunology, The University of Texas, M. D. Anderson Cancer Center, Houston, TX 77030
Even though all of the energy contained with the UV wavelengths of
solar radiation is absorbed within the epidermis and upper layers of
the dermis, UV irradiation can suppress immune responses to Ag
introduced at distant nonirradiated sites. In addition, data from a
number of laboratories have suggested that one consequence of UV
exposure is suppressed Th1 cell activation with normal or enhanced Th2
cell activation, resulting in a shift to a Th2-like phenotype.
Cytokines secreted by UV-irradiated keratinoctyes, particularly IL-10,
have been shown to play a major role in the induction of systemic
immune suppression and differential activation of T helper cell
subsets. Although IL-10 can influence Th1 cell activation by altering
Ag presentation and suppressing IFN-
secretion, the major signal for
the development of a Th2 response is IL-4. Here we tested the
hypothesis that UV irradiation induces IL-4 secretion. UV irradiation
induced serum IL-4 in a dose-dependent fashion. Injecting UV-irradiated
mice with anti-IL-4 blocked immune suppression. We could find no
evidence, however, supporting secretion of IL-4 by UV-irradiated
keratinocytes. Rather, we suggest that prostaglandins released by
irradiated keratinocytes induce serum IL-4 since treating UV-irradiated
mice with a cyclooxygenase-2 inhibitor blocked its production.
Moreover, we found that treating UV-irradiated mice with anti-IL-4
suppressed serum IL-10 levels. In addition, injecting normal mice with
PGE2 induced serum IL-4 and IL-10. We suggest that UV
exposure activates a cytokine cascade (PGE2 
IL-4
IL-10) that ultimately results in systemic immune suppression.
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