The immunosuppressive activity of ultraviolet light-B (UV-B) has become a major topic of interest, especially now that there are indications of an increased exposure to UV-B on the earth's surface, caused by a decreased thickness of the ozone layer. This review indicates that the thymus-dependent immune system is a prime target for damage by UV-B. Especially the systemic effects of UV-B on T cell mediated immunity are described and analyzed with respect to the mode of action. In summary, this review demonstrated that UV-B can alter T cell mediated immune responses by different pathways in which cytokines (e.g. TNF-alpha) and other soluble mediators (e.g. cis-urocanic acid) may play a role. Effects of UV-B on the location and morphology of different cells in the skin affect functionality of the immune system. Thus, UV-B may suppress local immunity against skin tumours and skin-associated infections as well as systemic immunity against non skin-associated infectious diseases and tumours.
"This circannual HPV rhythm is positively correlated with the annual sunlight fluency and UVB exposure at the global location of the screened population (Hrushesky et al., 2006). Ultraviolet B not only activates many viruses, both in vitro and in vivo, including HPV (Taylor et al., 2003), which causes human cervical cancer, but also suppresses cellular immune defenses against cancer and bacterial, fungal, parasitic , and viral infections, both locally and systemically (Goettsch et al., 1993; Bos, 1997; Selgrade et al., 1997). Annual rhythms in physiologic function have also been tied to regular seasonal daylight length changes in temperate latitudes (Farner, 1985; Sposito et al., 2000; Halberg et al., 2004; Hrushesky et al., 2005; Al-Tamer et al., 2008). "
[Show abstract][Hide abstract] ABSTRACT: Periodic episodes of increased sunspot activity (solar electromagnetic storms) occur with 10-11 and 5-6 year periodicities and may be associated with measurable biological events. We investigated whether this sunspot periodicity characterized the incidence of Pap smear-determined cervical epithelial histopathologies and human physiologic functions. From January 1983 through December 2003, monthly averages were obtained for solar flux and sunspot numbers; six infectious, premalignant and malignant changes in the cervical epithelium from 1,182,421 consecutive, serially independent, screening Pap smears (59°9″N, 4°29″E); and six human physiologic functions of a healthy man (oral temperature, pulse, systolic and diastolic blood pressure, respiration, and peak expiratory flow), which were measured ∼5 times daily during ∼34,500 self-measurement sessions (44°56″N, 93°8″W). After determining that sunspot numbers and solar flux, which were not annually rhythmic, occurred with a prominent 10-year and a less-prominent 5.75-year periodicity during this 21-year study span, each biological data set was analyzed with the same curve-fitting procedures. All six annually rhythmic Pap smear-detected infectious, premalignant and malignant cervical epithelial pathologies showed strong 10-year and weaker 5.75-year cycles, as did all six self-measured, annually rhythmic, physiologic functions. The phases (maxima) for the six histopathologic findings and five of six physiologic measurements were very near, or within, the first two quarters following the 10-year solar maxima. These findings add to the growing evidence that solar magnetic storm periodicities are mirrored by cyclic phase-locked rhythms of similar period length or lengths in human physiology and pathophysiology.
[Show abstract][Hide abstract] ABSTRACT: To assess the possibility that increases in UV-B exposure on the earth's surface could lead to impaired resistance to several infectious diseases, we studied the effect of UV-B exposure on resistance against Trichinella spiralis. Wistar rats, orally infected with T. spiralis larvae, were exposed to suberythemal doses of UV-B radiation daily for 5 days at different time periods before or after infection. A significant increase in the number of Trichinella larvae was found in the carcasses of rats irradiated with UV-B between 6 and 10 days after infection. These data indicate that exposure to UV-B radiation suppresses the resistance to a parasitic infection. We suggested that UV-B radiation especially suppresses cellular immune responses against these worms because specific IgM, IgG, and IgE titers were not significantly altered by UV-B exposure. These data indicate that UV-B irradiation plays a role in the course of infection with T. spiralis, which suggests that increases of UV-B exposure might also lead to problems with other infectious diseases and might affect vaccination because of the interaction of UV-B irradiation with memory T-cells.
Environmental Health Perspectives 04/1994; 102(3):298-301. DOI:10.1289/ehp.94102298 · 7.98 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Two types of antigen-specific T cells are needed for the elicitation of contact hypersensitivity reactions. They act in an obligate sequence to mediate the early initiating and late effector phases of contact hypersensitivity, which are accompanied by skin-swelling responses at 2 and 24 h after challenge, respectively. The magnitude of the late ear swelling depends on that of the early swelling.We studied the influence of ultraviolet radiation on both phases of contact hypersensitivity to picrylchloride. Mice were exposed to subedemal doses of ultraviolet radiation on the shaved backs for four consecutive days. Four days later mice were sensitized on non-irradiated skin. Four days after sensitization mice were challenged on the ears, and swelling was measured 2, 4, and 24 h after challenge. The early and late phases of contact hypersensitivity were largely suppressed in ultraviolet-irradiated, actively sensitized mice. Transfer of immune lymphoid cells from donor mice that were sensitized 4 d earlier induced early and late components of contact hypersensitivity in naive recipients after challenge. Transfer of immune lymphoid cells from donors that were sensitized 1 d earlier only induced the early component of contact hypersensitivity. Ultraviolet irradiation of donor mice significantly reduced the capacity of the immune lymphoid cells to induce contact hypersensitivity. We show that lymphoid cells responsible for the early and late components of contact hypersensitivity are both affected.Keywords: ultraviolet radiation, CHS, mice, photoimmunology
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