Suppression of Delayed and Contact Hypersensitivity Responses in Mice Have Different UV Dose Responses

Kim, Tae Heung; Ullrich, Stephen E.; Ananthaswamy, Honnavara N.; Zimmerman, Stuart O.; Kripke, Margaret L.

doi:10.1111/j.1751-1097.1998.tb02538.x

Cited by 48 publications

(27 citation statements)

References 26 publications

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“…This study also used a 310-nm UVB interference filter to ensure maximal UVB-only exposure without any UVC. In comparison, most other investigations 31 concerning CPD formation have used unfiltered FS40 sunlamps, which emit contaminating UVC. The enhanced potency of UVC in causing DNA damage may account for the variable importance of CPD at systemic low UVB doses.…”

Section: Discussionmentioning

confidence: 99%

Systemic Low-Dose UVB Inhibits CD8 T Cells and Skin Inflammation by Alternative and Novel Mechanisms

Rana

Rogers

Halliday

2011

The American Journal of Pathology

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Exposure to UVB radiation before antigen delivery at an unirradiated site inhibits functional immunological responses. Mice treated dorsally with suberythemal lowdose UVB and immunized with ova in abdominal skin generated ova-specific CD8 T cells with a significantly decreased activation, expansion, and cytotoxic activity compared with unirradiated mice. UVB also impaired the delayed-type hypersensitivity (DTH) reaction to ova. Transfer of CD4 ؉ CD25 ؉ cells from UVB-exposed mice did not suppress the ova-specific CD8 T-cell response or DTH reaction in unexposed mice, confirming that systemic low-dose UVB does not induce long-lived functional regulatory CD4 ؉ CD25 ؉ T cells. Repairing cyclobutane pyrimidine dimer-type DNA damage and blocking aryl hydrocarbon receptor signaling also did not reverse the immunosuppressive effect of UVB on ova-specific CD8 T cells and DTH, suggesting that cyclobutane pyrimidine dimers and the aryl hydrocarbon receptor are not required in systemic low-dose UVBinduced immunosuppression. The known UVB chromophore, cis-urocanic acid, and reactive oxygen species triggered the inhibition of DTH caused by UVB, but they were not involved in the modulation of CD8 T cells. These findings indicate that systemic low-dose UVB impedes the primary response of antigen-specific CD8 T cells by a novel mechanism that is independent of pathways known to be involved in systemic suppression of DTH. UVB radiation (290 to 320 nm) in natural sunlight is a potent immunosuppressant. UVB can inhibit the immune system from generating optimal responses to tumors, contact haptens, and various microbial antigens (Ags; viral, fungal, and parasitic) that can lead to exacerbated disease. Alternatively, immunosuppressive UVB can also be beneficial to control autoimmune diseases, such as psoriasis 1 and experimental autoimmune encephalomyelitis. 2 The epidermis of skin absorbs UVB through chromophores, including nuclear DNA, cytoplasmic tryptophan, and extracellular trans-urocanic acid (UCA). The molecular processes that follow trigger a cascade of events that cumulates in the phenomenon of UVB-induced immunosuppression. Some of the hallmarks of this immunosuppression include UVB-induced genetic mutations in skin cells, circulation of cis-UCA from the isomerization of trans-UCA, production of reactive oxygen species (ROS), and generation of regulatory T and B cells that can transfer suppression into UVB-naïve mice. 3 Because UVB has both detrimental and beneficial effects on the immune system, it is critical to understand the mechanisms regulated by UVB so that effective prophylactic and palliative therapies can be designed for skin diseases, such as skin cancer, and immune-mediated diseases in internal organs, such as multiple sclerosis.A previous study 4 showed that UVB can inhibit CD8 and CD4 T-cell responses to haptens. In a model of contact hypersensitivity (CHS), we demonstrated that a low dose of UVB (approximately 5 minutes of summer sunlight in Sydney, Australia, at midday) is sufficient to inhibit the activati...

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Section: Discussionmentioning

confidence: 99%

Systemic Low-Dose UVB Inhibits CD8 T Cells and Skin Inflammation by Alternative and Novel Mechanisms

Rana

Rogers

Halliday

2011

The American Journal of Pathology

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“…A 1,000 W xenon UV solar simulator equipped with a Schott WG-320 atmospheric attenuation filter (1 mm thick), a visible/IR band pass blocking filter (Schott UG-11; 1 mm thick), and a diachronic mirror to further reduce visible and IR energy (Oriel) was used to provide solar-simulated UV radiation (UVA + UVB, 290-400 nm). The intensity and spectral output of the WG-320-equipped solar simulator were measured with an Optronics model OL 754 scanning spectrophotometer (Optronics Laboratories), as described previously (15). Approximately 10% of the incident light was in the UVB (290-320 nm) portion of the spectrum.…”

Section: Methodsmentioning

confidence: 99%

Inhibition of Photocarcinogenesis by Platelet-Activating Factor or Serotonin Receptor Antagonists

et al. 2008

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The UV radiation in sunlight is the primary cause of nonmelanoma skin cancer. Moreover, UV exposure induces immune suppression. Early steps in the cascade of events leading to immune suppression are the binding of UVinduced platelet-activating factor (PAF) to its receptor and the binding of cis-urocanic acid, a photoreceptor for UVB radiation, to the serotonin (5-HT 2A ) receptor. Here, we tested the hypothesis that blocking the binding of PAF and 5-HT 2A to their receptors would also block skin cancer induction. Hairless mice were injected with PAF or serotonin receptor antagonists and then exposed to solar-simulated UV radiation. We noted a significant and substantial decrease in skin cancer incidence in mice treated with the PAF or 5-HT 2A receptor antagonists. Also, the PAF and/or serotonin receptor antagonists blocked skin cancer progression. The PAF and serotonin receptor antagonists worked in a synergistic fashion to block skin cancer induction. We also measured the effect that injecting PAF and 5-HT 2A receptor antagonists had on UV-induced skin damage after a single UV exposure. We noted a significant decrease in UV-induced hypertrophy, sunburn cell formation, and apoptosis when the mice were injected with PAF and/or 5-HT 2A receptor antagonists. These data indicate that treating UV-irradiated mice with PAF and 5-HT 2A receptor antagonists blocks skin cancer induction in vivo, in part by reversing UV-induced damage to the skin and by preventing the induction of immune suppression.

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“…The number of wrinkles in humans is significantly related to total hours of sun exposure in life [20] . In animal models, UVB radiation suppresses the immune response to hepatitis B vaccination, tuberculosis and leishmanial infection [21][22][23][24] and cutaneous delayed hypersensitivity [22,25,26] .…”

Section: Introductionmentioning

confidence: 99%

Sun-Induced Changes in Stratum Corneum Function Are Gender and Dose Dependent in a Chinese Population

Liu

Fluhr

Shu-min

et al. 2010

Skin Pharmacol Physiol

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Previous studies have demonstrated that UVB radiation changes the epidermal permeability barrier and stratum corneum (SC) hydration. It is well known that sun exposure causes erythema, sunburn and melanoma. However, whether daily sun exposure alters SC integrity and epidermal permeability barrier function is largely unknown, especially in Chinese subjects. In the present study, we assess the SC integrity, SC hydration and epidermal permeability barrier function following various doses of sun exposure. A total of 258 subjects (124 males and 134 females) aged 18–50 years were enrolled. A multifunctional skin physiology monitor (Courage & Khazaka MPA5) was used to measure SC hydration and transepidermal water loss (TEWL) on the forearms. In males, basal TEWL was higher with higher doses of sun exposure than with lower doses and control, whereas in females, basal TEWL was higher with lower doses of sun exposure than with higher doses and control. In the group with higher doses of sun exposure, TEWL in females was significantly lower than that in males. The barrier recovery was faster in females than in males in both control and lower-dose groups. In both males and females, barrier recovery was delayed with higher doses of sun exposure. In males, sun exposure did not alter SC hydration, while in females SC hydration was lower with lower doses of sun exposure as compared with control and higher doses of sun exposure. These results demonstrated that sun-induced changes in SC function and SC hydration vary with gender and the extent of sun exposure.

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Suppression of Delayed and Contact Hypersensitivity Responses in Mice Have Different UV Dose Responses

Cited by 48 publications

References 26 publications

Systemic Low-Dose UVB Inhibits CD8 T Cells and Skin Inflammation by Alternative and Novel Mechanisms

Systemic Low-Dose UVB Inhibits CD8 T Cells and Skin Inflammation by Alternative and Novel Mechanisms

Inhibition of Photocarcinogenesis by Platelet-Activating Factor or Serotonin Receptor Antagonists

Sun-Induced Changes in Stratum Corneum Function Are Gender and Dose Dependent in a Chinese Population

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