iLib08 - CitaviiLib08 - CitaviiLib08 - CitaviiLib08 - Citavi Andreu, G.; Boccaccio, C.; Leguen, J. P.; Oleggini, M. (1992): Ultraviolet light-induced immunomodulation: apossible new tool in organ transplantation. In: Annales de médecine interne, Jg. 143 Suppl 1, S. 52–56.SchlagwörterAdjuvants, Immunologic; Animals; Bloodradiation effects; Humans;Immunityradiation effects; Organ Transplantation; Ultraviolet RaysBöhm, M.; Luger, T. A. (2004): [Alpha-melanocyte-stimulating hormone. Its current significance for dermatology].In: Der Hautarzt; Zeitschrift für Dermatologie, Venerologie, und verwandte Gebiete, Jg. 55, H. 5, S. 436–445.Online verfügbar unter doi:10.1007/s00105-004-0729-0. AbstractAlpha-melanocyte-stimulating hormone (alpha-MSH) is a tridecapeptide that wasoriginally characterized as a neuropeptide derived from the pituitary gland. alpha-MSH is synthesized from pro-opiomelanocortin (POMC) by the action of specificprohormone convertases which cleave POMC into alpha-MSH, adrenocorticotropinand beta-endorphin. The various effects of alpha-MSH are mediated viamelanocortin receptors. The skin as well as the majority of cutaneous cell typesexpress POMC. Proinflammatory stimuli such as ultraviolet (UV) light induce POMCexpression and alpha-MSH secretion. Receptors for alpha-MSH are not onlyexpressed by melanocytes, where they mediate melanogenesis and proliferation,but also by virtually every cutaneous cell type. Accordingly, alpha-MSH elicits aplethora of biological actions in these cell types including immunomodulation,protection from oxidative stress and UV-induced apoptosis, modulation of secretoryepithelial function and regulation of extracellular matrix composition. These actionsmay be exploited in future by using super potent and truncated MSH peptides for the treatment of various skin disorders including inflammatory dermatoses.Schlagwörter Adjuvants, Immunologicmetabolism; Dermatologymethods; Humans;Melanocytesmetabolism; Pro-Opiomelanocortinmetabolism;Skinmetabolismradiation effects; Skin Diseasesdrug therapy; Ultraviolet Rays;alpha-MSHmetabolismtherapeutic useByrne, Scott N.; Ahmed, Jarin; Halliday, Gary M.: Ultraviolet B but not A radiation activates suppressor B cells indraining lymph nodes. In: Photochemistry and photobiology, Jg. 81, H. 6, S. 1366–1370. Online verfügbar unter doi:10.1562/2005-04-20-RA-495. AbstractImmunosuppressive doses of solar-simulated UV radiation activate lymph node Bcells that can suppress primary immunity by inhibiting the function of dendritic cells.The aim of this study was to determine the waveband responsible for activation of these suppressor B cells. We exposed C57BL/6 mice to various doses of either UVA or UVB radiation and analyzed the number and activation state of lymph nodeantigen-presenting cells (APC). Immunosuppressive doses of UVB but not UVAactivated B cells as assessed by major histocompatibility complex II (MHC II)expression and doubled their numbers in draining lymph nodes. Higher doses of UVA that were not immunosuppressive actually suppressed B cell activation. Our results show that UVA and UVB suppress systemic immunity via differentmechanisms. Lymph node B cells are activated in response to immunosuppressivedoses of UVB but not UVA. Thus, the activation state of lymph node APC appearsto be important for UV immunomodulation.Schlagwörter Animals; B-Lymphocytescytologyimmunologyradiation effects; DendriticCellscytologyimmunologyradiation effects; Female; Immune Tolerance; LymphNodesimmunology; Lymphocyte Activation; Mice; Mice, Inbred C57BL; UltravioletRaysCooper, Kevin D.; Baron, Elma D.; Matsui, Mary S. (2003): Implications of UV-induced inflammation andimmunomodulation. In: Cutis; cutaneous medicine for the practitioner, Jg. 72, H. 3 Suppl, S. 11-5; discussion 16. AbstractSunscreens are the most effective and widely available interventions for sundamage, other than sun avoidance or clothing. However, sun-screens vary widely intheir ability to screen various UV wavelength components. Testing methods for sunscreens rely on UV-induced erythema to determine a sun protection factor

iLib08 - CitaviiLib08 - CitaviiLib08 - CitaviiLib08 - Citavi(SPF), primarily a measure of UVB protection only. Determination of an immuneprotection factor (IPF) has been proposed as an alternative or adjunctive measureto SPF, and, indeed, recent studies show that the IPF can detect the added in vivofunctionality of sunscreens--such as high levels of UVA protection--that the SPFcannot. Consensus on the definition of IPF, however, is required. Data are availableon quantification of the IPF for restoring the afferent or induction arm of contactsensitivity, but other immune parameters also have been measured. A review of invivo studies in humans, in which sunscreens are used to intervene in UV-inducedmodulation of immune response, cells, or cytokines, highlights the technicalvariables and statistical approaches that must be standardized in the context of anIPF for regulatory product claim purposes. Development of such IPF standardswould allow the integration of both UVB and non-UVB solar wave-band effect-reversals. In addition, it could be applied to integrate the effects of other ingredientswith protective function (ie, antioxidants, retinoids, or other novel products) and spur the development of more advanced and complete protection products.Schlagwörter Humans; Inflammationetiologyimmunologypathology; Skinimmunologyradiationeffects; Sunscreening Agentspharmacology; Ultraviolet Raysadverse effectsGarssen, J.; van Loveren, H. (2001): Effects of ultraviolet exposure on the immune system. In: Critical reviews inimmunology, Jg. 21, H. 4, S. 359–397. AbstractDepletion of stratospheric ozone and changes in lifestyle lead to an increasedexposure to ultraviolet (UV) wavebands, especially in the UVB region (280-320 nm).Besides the beneficial effects of UV exposure, such as vitamin D production,cosmetic tanning, and adaptation to solar UV, UV exposure can also have adverseconsequences on human health, notably sunburn, skin cancer, and ocular damage.Over the last two and a half decades it has become evident that especially UVBexposure and to a lesser extent UVA modulates specific as well as nonspecificimmune responses. Several reports have shown that this immunomodulation playsat least a partial role in the induction of skin cancer. In addition, UVB exposure hasbeen demonstrated to impair resistance to some infections. On the other hand,immunomodulation resulting from UVB exposure might be physiologically importantin inhibiting responses to neoantigens in the skin induced by UV exposure. In thelast 20 years UV has been used frequently as an experimental tool to unravelimmune responses-especially immune responses initiated in the skin (i.e.,photoimmunology). In this review, the major mechanisms responsible for UV-induced immunomodulation and its consequences are summarized.Schlagwörter Animals; Cytokinesimmunology; Humans; Immune Systemradiation effects;Photoreceptor Cellsimmunology; Ultraviolet RaysHart, P. H.; Grimbaldeston, M. A.; Finlay-Jones, J. J.: Sunlight, immunosuppression and skin cancer: role of histamine and mast cells. In: Clinical and experimental pharmacology & physiology, Jg. 28, H. 1-2, S. 1–8. Abstract1. The development into tumours of skin cells transformed by ultraviolet (UV) Bradiation of wavelengths 290-320 nm is enhanced by the ability of UVB to suppressan immune response that would otherwise destroy them. Ultraviolet B-inducedimmunomodulation may be by multiple mechanisms, but generally manifests in anantigen-presenting cell defect and an altered cytokine environment in the draininglymph nodes. 2. Immune responses to microbial or self-antigens may bedysfunctional by similar mechanisms following UVB exposure. 3. Earliest-actingintermediates in the initiation of UVB-induced immunosuppression are the UVBabsorbers (photoreceptors) of the skin, notably DNA resulting in immunoregulatorycytokine production, and trans-urocanic acid (UCA), which, upon isomerization to itscis isomer, signals downstream immunosuppressive events. 4. In mice, dermalmast cells are critical to UVB-induced systemic immunomodulation. In mice, there isa functional link as well as a linear relationship between the prevalence of histamine-staining dermal mast cells and the log of the dose of UVB required for 50% immunosuppression. Studies with histamine receptor antagonists support

iLib08 - CitaviiLib08 - CitaviiLib08 - CitaviiLib08 - Citavihistamine as the main' product of mast cells involved. Histamine acts in large partvia a prostanoid-dependent pathway. 5. Approximately 50% of humans and greater than 90% of patients with non-melanoma skin cancer are UVB susceptible for suppression of a contact hypersensitivity response. Neither cytokine polymorphismsnor UVB-induced levels of cis-UCA in irradiated skin have been linked to UVBsusceptibility. Patients with basal cell carcinomas (BCC) have an increased dermalmast cell prevalence in non-sun-exposed buttock skin. We propose that mast cellsfunction in humans, as in mice, by initiating immunosuppression and, thereby,allowing a permissive environment for BCC development.Schlagwörter Animals; Carcinoma, Basal Cellimmunologymetabolism; Dermatitis,Contactimmunologymetabolism; Histamineimmunologymetabolismradiation effects;Humans; Immunosuppression; Mast Cellsimmunologymetabolismradiation effects;Mice; Neoplasms, Radiation-Inducedimmunologymetabolism; SkinNeoplasmsimmunologymetabolism; Ultraviolet Raysadverse effectsHart, P. H.; Grimbaldeston, M. A.; Finlay-Jones, J. J.: Mast cells in UV-B-induced immunosuppression. In:Journal of photochemistry and photobiology. B, Biology, Jg. 55, H. 2-3, S. 81–87. AbstractDegranulating dermal mast cells in UV-B-irradiated skin have been implicated for many years in the mechanisms of irradiation erythema. There is now considerableevidence that dermal mast cells are important to the processes by which both UV-Bradiation and cis-urocanic acid (cis-UCA) suppress immune responses tosensitizing antigens applied to non-irradiated/non-cis-UCA-exposed sites. Mast-cell-depleted mice are resistant to the immunosuppressive effects of UV-B radiation andcis-UCA for 'systemic' immunomodulation. However, these mice gainresponsiveness if the dorsal skin is reconstituted six weeks prior to irradiation or cis-UCA administration at that site with cultured bone-marrow-derived mast cells from+/+ mice. The molecular triggers for initiating mast-cell degranulation are beingactively sought. Evidence suggests that histamine, and not tumour necrosis factor alpha, is the major mast-cell product that signals altered immune responses tosensitizing antigens applied to non-irradiated, non-cis-UCA-exposed sites.Histamine may have multiple roles, but experiments with indomethacinadministered to mice have shown that one process involves induction of prostanoidproduction.Schlagwörter Animals; Bone Marrow Cellscytology; Immunosuppression; Mast Cellsdrugeffectsimmunologyradiation effects; Mice; Skindrug effectsimmunologyradiationeffects; Ultraviolet Rays; Urocanic AcidpharmacologyHurks, H. M.; van der Molen, R. G.; Out-Luiting, C.; Vermeer, B. J.; Claas, F. H.; Mommaas, A. M. (1997):Differential effects of sunscreens on UVB-induced immunomodulation in humans. In: The Journal of investigative dermatology, Jg. 109, H. 6, S. 699–703. Online verfügbar unter doi:10.1111/1523-1747.ep12340652. AbstractUltraviolet radiation has been shown to suppress the (skin) immune system both inanimal species and in humans. Whether sunscreens can preventimmunosuppression is a matter of debate. This study investigated the protectivecapacity of a commercial sunscreen lotion in humans. Part of the right arm of healthy volunteers was exposed to erythemagenic ultraviolet B doses of 160 mJ per cm2 for four consecutive days. Before irradiation, sunscreen was applied either directly onto the skin or onto a piece of quartz fixed to the skin (to avoid penetrationof the sunscreen in the epidermis where it cannot block the photoisomerization of trans-urocanic acid in cis-urocanic acid in the stratum corneum). The control groupwas irradiated without prior application of sunscreen. Four h after the lastirradiation, epidermal sheets were obtained by the suction-blister method from botharms and epidermal cells were used as stimulator cells in the mixed epidermal celllymphocyte reaction. Responses directed to epidermal cells derived from irradiatedskin were expressed as percentages of responses directed to epidermal cellsderived from the nonirradiated left arm. The mixed epidermal cell lymphocyte