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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Experimental dermatology 1 (1992), S. 0 
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract The purpose of this study was to determine whether exposing mice to ultraviolet radiation (UVR) would alter the pathogenesis of infection with Mycobacterium lepraemurium (MLM), which causes a chronic, progressive, lethal disease in susceptible mouse strains. BALB/c mice were irradiated on dorsal skin with various doses of UVR from FS40 sunlamps 3 days before infection with MLM in the hind footpad. The course of disease was followed by assessing the number of acid-fast bacteria in the footpad, regional lymph node and spleen, and measuring the size of the lesion at the site of MLM infection at various times after infection. Mice were also tested periodically for a delayed-type hypersensitivity (DTH) response by injecting MLM antigen into the uninfecled footpad and measuring footpad swelling 24 hours later. Mice treated with a single high dose of UVR (45 kJ/m2) had significantly more bacteria in the infected footpad, lymph node and spleen than unirradiated control animals. They also had larger lesions at the site of MLM infection and exhibited significant suppression of the DTH response at 3 and 6 months after infection. Injection of mice s.c. in the footpad with MLM 3 d after 45 kJ/m2 UVR reduced the median survival time from 391 to 305 d and after i.v. infection from 171 to 139 d. Dose-response studies indicated that exposing mice to 2.3 kJ/m2 of UVR, which is approximately 1 minimal erythemal dose for this strain, suppressed the DTH response by 50% at 3 months alter infection. Significant increases in the number of bacteria in the footpad, spleen and lymph node were detected with doses of UVR≥5.6 kJ/m2. Mice exposed chronically to UV radiation also showed impaired responses to MLM. Thus, exposing mice to a single or multiple doses of UVR before infection increased the severity of a chronic mycobacterial infection and decreased the immune response to mycobacterial antigens.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Experimental dermatology 1 (1992), S. 0 
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract Injection of melanoma cells into the UV-irradiated ear skin of syngeneic mice results in an increased incidence of melanomas compared with that in nonirradiated ear skin. This effect of UV is localized to the site of irradiation and appears to be immunoiogically mediated. In these studies we test the hypothesis that the effect of UV irradiation on melanoma development is related to its ability to alter epidermal Langerhans cells and impair the induction of contact hypersensitivity. A regimen of UV irradiation that altered epidermal immune cells and interfered with the generation of contact hypersensitivity was tested for its ability to increase the incidence of melanoma. Conversely, the ear skin of C3H mice treated with a regimen of UV radiation that enhanced melanoma development was examined for the number of appearance of ATPase+ and Thy-1+ dendritic epidermal cells and tested for the ability to initiate a contact hypersensitivity response. No correlation between these effects of UV irradiation could be detected. Furthermore, implantation of melanoma cells into UV-irradiated ear skin resulted in the generation of systemic immunity against subsequent tumor challenge. Therefore, we conclude that the ability of UV irradiation to modify melanoma development is unrelated to its effects on the afferent arm of the contact hypersensitivity response and that enhanced melanoma development is not due to an impairment in the induction of tumor immunity.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract Exposure of mice to UVB radiation down-regulates the induction of contact hypersensitivity (CHS) responses to haptens applied to the site of irradiation. Concomittantly, the activity of antigen-presenting cells (APC) in the draining lymph nodes is decreased, and T lymphocytes that suppress the induction of CHS are induced. We assessed the röle of DNA damage in modulation of the CHS response by UV irradiation by applying liposomes containing T4 endonuclease V (T4N5) to the UV-irradiated skin. Liposomal T4N5. which increases the rate of repair of cyclobutyl pyrimidine dimers (CPD) in DNA. prevented the reduction in the CHS response, the impairment in APC function, and the induction of transferrable immune suppression. Liposomes containing heat-inactivated T4N5 did not restore immune responsiveness. In this model, hapten-bearing APC from unirradiated mice also fail to induce CHS upon injection into UV-irradiated recipients. This systemic effect of UV irradiation on APC function was also prevented by application of liposomes containing active, but not inactive, T4N5. These studies support the hypothesis that DNA damage is an essential initiator of one or more steps leading to impaired immune responsiveness after UV irradiation. They further imply that the release of cytokines that modulate APC function after UV irradiation is triggered by DNA damage.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science, Ltd
    Experimental dermatology 11 (2002), S. 0 
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The relationship between exposure to UVB radiation and development of skin cancer has been well established. Several studies have shown that UVB induces unique mutations (C to T and CC to TT transitions) in the p53 tumor suppressor gene that are not commonly induced by other carcinogens. Our studies have demonstrated that UV-induced mouse skin cancers contain p53 mutations at a high frequency and that these mutations can be detected in UV-irradiated mouse skin well before the appearance of skin tumors. This observation suggested that it might be possible to use p53 mutations as a biological endpoint for testing the efficacy of sunscreens in photoprotection studies. Indeed, application of SPF 15 sunscreens to mouse skin before each UVB irradiation resulted in 88–92% reduction in the number of p53 mutations. Because p53 mutations represent an early essential step in photocarcinogenesis, these results imply that inhibition of this event may protect against skin cancer development. This hypothesis is confirmed by our finding that sunscreens used in p53 mutation inhibition experiments also protected mice against UVB-induced skin cancer.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science, Ltd
    Experimental dermatology 11 (2002), S. 0 
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The ultraviolet (UV) radiation present in sunlight is immune-suppressive. Recently we showed that solar-simulated UV radiation (UVA + UVB; 295–400 nm), applied after immunization, suppressed immunological memory and the elicitation of delayed-type hypersensitivity to the common opportunistic pathogen, Candida albicans. Further, we found that wavelengths in the UVA region of the solar spectrum (320–400 nm), devoid of UVB, were equally effective in activating immune suppression as UVA + UVB radiation. Here we report on the mechanisms involved. No immune suppression was found in UV-irradiated mice injected with monoclonal anti-interleukin (IL)-10 antibody, or mice exposed to solar-simulated UV radiation and injected with recombinant IL-12. Antigen-specific suppressor T cells were found in the spleens of mice exposed to UVA + UVB radiation. Applying liposomes containing bacteriophage T4N5 to the skin of mice exposed to solar-simulated UVA + UVB radiation or mice exposed to UVA radiation blocked immune suppression, demonstrating an essential role for UV-induced DNA damage in the suppression of established immune reactions. These findings indicate that UV radiation activates similar immunological pathways to suppress the induction, or the elicitation, of the immune response.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Immunological reviews 80 (1984), S. 0 
    ISSN: 1600-065X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1546-170X
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] UV-induced mutations in the p53 tumor suppressor gene play an essential role in skin cancer development. We report here that such mutations can be detected in UV-irradiated mouse skin months before the gross appearance of skin tumors. Application of SPF-15 sunscreens to mouse skin before each UV ...
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature genetics 34 (2003), S. 23-23 
    ISSN: 1546-1718
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Ramaswamy et al. compared gene expression profiles of adenocarcinoma metastases to unmatched primary adenocarcinomas. They found an expression pattern that distinguished primary tumors from metastases but also reported that a subset of primary tumors had the expression pattern of metastases. This ...
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    British journal of dermatology 122 (1990), S. 0 
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The effect of photochemotherapy with 4,4′,6 trimethylangelicin (TMA), a new monofunctional furocoumarin with a high antiproliferative activity, was studied on murine dendritic epidermal cells. Female mice (C3H/HeN[MTV-]) were treated topically with the drug three times a week for 4 consecutive weeks followed each time by I J/cm2 of UVA radiation. At the end of the treatment almost total depletion of ATPase+, Ia+ and Thy-I+ dendritic epidermal cells was observed, associated with marked hyperpigmentation but no gross or microscopic phototoxicity. Although 4,4′,6 TMA is not phototoxic in mice, it affects the cutaneous immune cells.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 392 (1982), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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