[Nle4-D-Phe7]-alpha-melanocyte-stimulating hormone significantly increased pigmentation and decreased UV damage in fair-skinned Caucasian volunteers.

Epidermal melanin reduces some effects of UV radiation, the major cause of skin cancer. To examine whether induced melanin can provide protection from sunburn injury, 65 subjects completed a trial with the potent synthetic melanotropin, [Nle4-D-Phe7]-alpha-melanocyte-stimulating hormone ([Nle4-D-Phe7]-alpha-MSH) delivered by subcutaneous injection into the abdomen at 0.16 mg/kg for three 10-day cycles over 3 months.

The induction of immunity to a protein antigen using an adjuvant is significantly compromised by ultraviolet A radiation.

Ultraviolet (UV) radiation from sunlight causes skin cancer and inhibits priming of the immune system during vaccination. However the dose related effects of the different components of sunlight (UVA and UVB) are complex and require further investigation. Using ovalbumin as a model protein vaccine with saponin as adjuvant we show that both UVA and UVB can suppress the DTH response to a poorly immunogenic protein.

Sunlight-induced immunosuppression in humans is initially because of UVB, then UVA, followed by interactive effects.

Solar-simulated ultraviolet radiation (ssUV) suppresses immunity in humans. The ultraviolet B (UVB) waveband is recognized as immunosuppressive; however the relative significance of UVA to ssUV immunosuppression is unknown. We created dose and time-response curves for UVB-, UVA-, and ssUV-induced suppression of memory immunity to nickel in humans.

Ultraviolet B but not A radiation activates suppressor B cells in draining lymph nodes.

Immunosuppressive doses of solar-simulated UV radiation activate lymph node B cells 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 node antigen-presenting cells (APC).

Inflammation, gene mutation and photoimmunosuppression in response to UVR-induced oxidative damage contributes to photocarcinogenesis.

Ultraviolet (UV) radiation causes inflammation, gene mutation and immunosuppression in the skin. These biological changes are responsible for photocarcinogenesis. UV radiation in sunlight is divided into two wavebands, UVB and UVA, both of which contribute to these biological changes, and therefore probably to skin cancer in humans and animal models.

B cells activated in lymph nodes in response to ultraviolet irradiation or by interleukin-10 inhibit dendritic cell induction of immunity.

Ultraviolet (UV) radiation suppresses systemic immunity. We explored these cellular mechanisms by exposing mice to systemically immunosuppressive doses of UV radiation and then analyzing cell phenotype and function in the lymphoid organs. Although UV radiation increased total cell number in the draining lymph nodes (DLN), it did not alter the activation state of dendritic cells (DC).

The suppression of immunity by ultraviolet radiation: UVA, nitric oxide and DNA damage.

We have examined the mechanism by which solar-simulated ultraviolet radiation (ssUV) suppresses memory immunity to nickel in allergic humans. In initial studies, we used inbred mice to determine the contribution of different wavebands to sunlight-induced immunosuppression. We found that low dose UVA can enhance memory, medium dose UVA (half the amount in one minimum erythemal dose of ssUV) is immunosuppressive, but higher doses protect from UVB.

Increased Fas ligand expression by T cells and tumour cells in the progression of actinic keratosis to squamous cell carcinoma.

Background: In the counterattack model of tumorigenesis, it has been proposed that tumours develop resistance to attack from Fas ligand (FasL)-expressing cytotoxic T cells by downregulating Fas (immune escape), while at the same time upregulating FasL expression to induce apoptosis in Fas-expressing T cells (counterattack).

Objectives: The aim of this study was to examine Fas and FasL expression on tumour cells and infiltrating T cells during the progression of actinic keratoses (AK), the benign precursor lesion, to squamous cell carcinoma (SCC).

Patients And Methods: Samples of AK (n = 20) and SCC (n = 20) were collected from immunocompetent patients attending dermatology clinics.

Nitric oxide appears to be a mediator of solar-simulated ultraviolet radiation-induced immunosuppression in humans.

Topical application of NG-methyl-L-arginine and 2,2'-dipyridyl were used to examine the respective roles of nitric oxide and reactive oxygen species in solar-simulated ultraviolet radiation-induced immunosuppression in humans in vivo. Immunosuppression was studied using a nickel contact hypersensitivity recall model. Ultraviolet radiation dose-responses were generated to determine the extent to which NG-methyl-L-arginine and 2,2'-dipyridyl affected the immune response.

Phagocytosis by dendritic cells rather than MHC IIhigh macrophages is associated with skin tumour regression.

Dendritic cells (DC) are important for the induction of anti-tumour immunity and are currently being used in clinical trials. Whether DC in tumours behave the same as DC in normal tissues or whether the tumours subvert DC phenotype and function remains unknown. To address this, we have used a unique animal tumour model to compare the DC infiltrating regressing tumours with the DC infiltrating progressing skin tumours.

Prevention of immunosuppression by sunscreens in humans is unrelated to protection from erythema and dependent on protection from ultraviolet a in the face of constant ultraviolet B protection.

Sunscreens have been advocated as an important means of preventing skin cancer. Ultraviolet radiation induced immunosuppression is recognized as an important event in skin cancer development, yet the effectiveness of sunscreens in protecting the human immune system from ultraviolet radiation (i.e.

High levels of Fas ligand and MHC class II in the absence of CD80 or CD86 expression and a decreased CD4+ T cell Infiltration, enables murine skin tumours to progress.

It is still not clear why some tumours will be recognized and destroyed by the immune system, and others will persist, grow, and eventually kill the host. It has been hypothesized that tumour cells might evade immunological destruction by expressing Fas ligand (FasL), a molecule which induces apoptosis in Fas(+) target cells. However, the role of FasL in creating an immune privileged status within a tumour remains controversial.

Dendritic cells: making progress with tumour regression?

Due to their potent ability to activate the immune system, dendritic cells (DC) are showing promise as potential adjuvants for tumour immunotherapy of cancer patients. However, little is known about the effect tumour cells can have on DC function. Indeed, the discovery of different DC subsets with different immunological functions indicates that the relationship between tumour cells and tumour-infiltrating DC subtypes is likely to be complex.

Ultraviolet a irradiation of C57BL/6 mice suppresses systemic contact hypersensitivity or enhances secondary immunity depending on dose.

Ultraviolet radiation is the most common environmental carcinogen humans are exposed to. It is now known that in order for skin cancers to develop, both genetic damage and immunosuppression is required. Ultraviolet-induced immunosuppression is therefore a key contributor to the development of skin cancer.

The importance of using broad spectrum SPF 30+ sunscreens in tropical and subtropical climates.

Background/purpose: To evaluate the Sun Protection Factors (SPF) of six sunscreens sold in Australia, using an ultraviolet (UV) spectrum which mimics sunlight as closely as possible, and by using volunteers with a range of skin types to reflect the Australian population.

Methods: Open prospective study. Seventy-five volunteers of skin types 1-3 were tested in a dermatology research laboratory in a major metropolitan teaching hospital in Sydney, Australia in the years 2000-2001.

Measurement of ultraviolet radiation-induced suppression of recall contact and delayed-type hypersensitivity in humans.

This article describes methodology used for assessment of ultraviolet radiation-induced suppression of recall responses in humans. Nickel allergy is common in the general population and patch testing of nickel-allergic volunteers provides a convenient model of contact hypersensitivity. Similarly, Mantoux-positive volunteers, recruited from within hospital staff, are used as a model for delayed-type hypersensitivity.