There is good evidence both in humans and experimental animals that ultraviolet radiation causes local (that is, occurring only at the site of irradiation) and systemic immunosuppression. Although the mechanisms of ultraviolet radiation-induced immunosuppression are better understood, many questions remain to be answered. The consequences of immunosuppression for patterns of infectious disease in human populations are less clear.
Cellular immunity and the activity of natural killer cells have been shown to be affected by ambient doses of ultraviolet radiation (159). Ultraviolet radiation-induced suppression may therefore play a role in reduced resistance to skin tumours. Immunosuppression may also lead to diminished resistance to viral and bacterial infections because, in addition to the activity of natural killer cells and cellular immunity, phagocytic activity is also reduced. All these mechanisms are involved in immune resistance to infections. Such effects have been shown in experimental laboratory animals. Animal data can be extrapolated to humans with information from studies that compare species. The results from such extrapolation studies indicate that ambient doses of ultraviolet radiation reduce the resistance to infectious diseases in humans (160). The effect of ultraviolet radiation on herpes simplex infection is well known and confirms the effects found in animal studies.
Further epidemiological studies are required to fully understand the impact on the incidence and prevalence of infections. Even a modest effect on the immune system that may result in a moderate depression of resistance to an infection, or affect its duration or severity, may have a significant aggregate social and economic impact at the population level for very common diseases (such as the common cold and gastroenteritis).
Ultraviolet radiation-induced changes in immune response may also affect autoimmune diseases. Increases in ultraviolet radiation may either suppress or aggravate the disease depending on the type of immune response that underlies the disease. It has recently been proposed, based on epidemiological and laboratory evidence, that increased exposure to ultraviolet radiation is associated with a lower prevalence of multiple sclerosis (161). It is also known that ultraviolet radiation aggravates lupus lesions when used as a medical treatment (54).
It is now generally accepted that allergic respiratory disease (such as asthma) is associated with the enhanced expression of the Th2 cell pathway immune response (162). Ultraviolet radiation has been shown to preferentially suppress the Th1 component of the cellular immune response and to enhance the Th2 component. It has also been suggested that production of immunoglobulin E (IgE) - the immunoglobulin involved in the immediate hypersensitivity immune (allergic) response - is stimulated by ultraviolet radiation in experimental animals (159,163). The detrimental effect of ultraviolet radiation on lupus, which is a Th2-type phenomenon, supports the argument for this mechanism in humans. The stimulation of the Th2 response by ultraviolet radiation, and hence stimulation of IgE production, may result in respiratory allergy. Increased exposure to ultraviolet radiation, such as from lifestyle and personal behaviour, may thus play a role in the as yet unexplained increase in the prevalence of respiratory allergy in many countries.
By affecting the immune system, an increase in ultraviolet radiation may have important effects on the incidence and prevalence of infectious diseases. It may also have important effects on autoimmune and atopic diseases. Climate change may also affect the distribution of pathogens and allergens as well as other factors that affect the immune system, such as natural toxins from moulds that contaminate wheat. Such phenomena may well interfere with and influence the consequences of immunosuppression.
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