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Suberythemal ultraviolet radiation (UVR) exposures of children are used routinely in Russia to prevent rickets and to strengthen general health. The aim of the present study was to re-evaluate the effects of such a regime on immune responses as UVR is now recognised to suppress cell-mediated immunity in many animal models. Seventeen infants were immunised with attenuated measles and recall polio vaccines of whom 10 had been given a course of prophylactic UV exposures before the vaccinations. All the infants in the study developed an acute infectious conjunctivitis one week prior to the vaccinations and were convalescent at the time of the vaccination. They were bled on the day of the vaccinations and at several times thereafter to assess leukocyte percentages and plasma cytokine levels. On the day of the vaccinations, an active immune response was apparent. The UV-exposed children differed from the unexposed children by having a smaller percentage of natural killer cells and a higher percentage of CD25-positive cells. In the days following the vaccinations, the UV-exposed infants had a lowered percentage of total lymphocytes with increased percentages of monocytes, eosinophils, neutrophils and HLA-DR-positive cells as well as higher concentrations of plasma IL-1beta and IL-10 compared with the unexposed infants. There were no local or systemic clinical reactions to the vaccines in the UV-group while a moderate rise in temperature of three children in the unexposed group occurred. Thus the UV irradiations modulated leukocyte percentages and plasma cytokine levels following the vaccinations, perhaps through the activation of a T helper 2-like response.

Studies of UV-induced skin cancers show that malignisation of skin cells, as well as alterations in anti-tumor immune control, are triggered by UV-induced lesions in cellular DNA. Such lesions can probably appear in the human mononuclear leukocytes (lymphocytes) during exposure of skin to sunlight. With the aim of studying the processing of UV-induced DNA lesions in these cells, we used flow cytometry and labelling of their partially denatured nuclei with the monoclonal antibody (H3) that binds cyclobutane pyrimidine dimers in single-stranded DNA. After the first few hours of cultivation of the irradiated cells, we found an increase in H3-specific fluorescence from cellular nuclei, while there was a decrease in the number of H3-positive sites in isolated DNA from these cells. We examined cells cultured under different conditions and concluded that the effect of enhancement of H3 labelling of nuclei did not result from changes in temperature and culture medium. Furthermore, we have found that this effect, as well as the decrease in H3 labelling in isolated DNA, are both prevented by pretreatment of the cells with Novobiocin, which we used as an inhibitor for the topoisomerase II-induced relaxation of supercoiled DNA prior to repair-specific incision. The inhibition by Novobiocin of the above-mentioned changes in H3 labelling in cellular nuclei and isolated DNA of the irradiated cells clearly indicate the association of both effects with an excision repair-related DNA modification. While the partial loss of H3-binding sites from isolated DNA is obviously a result of excision of some fraction of pyrimidine dimers, the enhancement of the H3 labelling of nuclei might be due to the formation of open structures at dipyrimidine-containing DNA fragments in preparation for incision. We suggest that formation of open structures predominates quantitatively over dual incision and excision of these fragments, and leads to enhanced exposure of the pyrimidine dimers in nuclei to H3 binding. Thus, unstimulated human lymphocytes appear to be capable of performing pre-incision steps for removal of these DNA lesions.

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