This study detected and compared the levels of Il-17A, IFN-gamma and IL-10 in the amniotic fluid (AF) and serum of pregnant women with acute toxoplasmosis in southern Brazil. It also compared the serum levels of these mediators in pregnant women with acute or chronic toxoplasmosis and with uninfected women. The serological investigations of anti-T. gondii IgM and IgG from the 60 pregnant women were determined by chemiluminescence microparticle immunoassay (CMIA). Twenty patients were uninfected, twenty were in the chronic phase and twenty were in the acute phase of toxoplasmosis. The 20 pregnant women in acute phase all agreed with amniocentesis. Serum and AF cytokines were evaluated by sandwich enzyme-linked immunosorbent assay. The analyzed cytokines showed no significant difference in blood versus amniotic fluid levels of pregnant women in the acute toxoplasmosis. Furthermore, we observed that serum IL-17A was significantly higher in pregnant women in the acute phase of infection compared to pregnant women with chronic toxoplasmosis and seronegative pregnant women. T. gondii DNA was not amplified in any of the samples of amniotic fluid by the nested-PCR reaction. Serum IL-10 levels were also higher in negative pregnant women than in infected pregnant women. Our findings indicate the activation of an inflammatory response to infection by T. gondii and suggest that increased production of IL-17A may be a protective factor against infection of the fetus.

UV-based phototherapy (including psoralen plus UVA (PUVA), UVB and UVA1) has a long, successful history in the management of numerous cutaneous disorders. Photoresponsive diseases are etiologically diverse, but most involve disturbances in local (and occasionally systemic) inflammatory cells and/or abnormalities in keratinocytes that trigger inflammation. UV-based phototherapy works by regulating the inflammatory component and inducing apoptosis of pathogenic cells. This results in a fascinating and complex network of simultaneous events-immediate transcriptional changes in keratinocytes, immune cells, and pigment cells; the emergence of apoptotic bodies; and the trafficking of antigen-presenting cells in skin-that quickly transform the microenvironment of UV-exposed skin. Molecular elements in this system of UV recognition and response include chromophores, metabolic byproducts, innate immune receptors, neurotransmitters and mediators such as chemokines and cytokines, antimicrobial peptides, and platelet activating factor (PAF) and PAF-like molecules that simultaneously shape the immunomodulatory effects of UV and their interplay with the microbiota of the skin and beyond. Phototherapy's key effects-proapoptotic, immunomodulatory, antipruritic, antifibrotic, propigmentary, and pro-prebiotic-promote clinical improvement in various skin diseases such as psoriasis, atopic dermatitis (AD), graft-versus-host disease (GvHD), vitiligo, scleroderma, and cutaneous T-cell lymphoma (CTCL) as well as prevention of polymorphic light eruption (PLE). As understanding of phototherapy improves, new therapies (UV- and non-UV-based) are being developed that will modify regulatory T-cells (Treg), interact with (resident) memory T-cells and /or utilize agonists and antagonists as well as antibodies targeting soluble molecules such as cytokines and chemokines, transcription factors, and a variety of membrane-associated receptors.

Chronic actinic dermatitis (CAD) has a more complicated pathogenetic basis than others. The clinical grading system and its correlations with the clinical and immunological parameters still remained to be investigated to define the nature of CAD in a more detailed manner.

We investigated correlations of the clinical severity score of CAD (CSS-CAD) with the clinical and immunological parameters.

We evaluated 72 patients with CAD and classified them into three groups according to the CSS-CAD. We analysed total IgE level, peripheral blood (PB) eosinophil count, the ratio of Th2cell (CCR4 + CD4 +) percentage over Th1 cell (CXCR3 + CD4 +) percentage (Th2/Th1) and/or the sum of suppressor/cytotoxic T cells.

The total IgE levels and the percentage of PB eosinophils were higher in the severer group than other groups. A shift towards Th2 from Th2/Th1 balanced status may be affected by total counts of suppressor T cells, and the patient with higher Th2/Th1 ratio than balanced status had the more proportion in the severer CSS-CAD group than other groups.

The CSS-CAD correlates with total IgE level, PB eosinophil count and a shift towards Th2 immunity from Th2/Th1. So we suggest the Th1/Th2 dysbalance may be affected by the CSS-CAD.

We herein compared the effects of the chronic feeding of high-fat (HF), high-sucrose (HS), and low-fat/low-sucrose (control) diets on carcinogenesis following chronic ultraviolet B (UVB) irradiation in hairless mice. UVB irradiation-induced carcinogenesis was more prominent in HF diet-fed group than in control diet- and HS diet-fed groups. The HS diet group, as well as the HF diet one, showed tumor development and growth, increased skin matrix metalloproteinase (MMP) and blood plasminogen activator inhibitor-1 (PAI-1) levels, and decreased blood leptin and adiponectin levels after long-term UVB irradiation. These changes were smaller in the HS diet group than in the HF diet group. In addition, no difference was noted in the above changes between the control and HS diet groups. The increase induced in adipose tissue weight by the HF diet was markedly reduced by UVB irradiation. This result suggests that the abundant availability of lipids in hypertrophic adipose tissue may be related to tumor incidence and growth through increases in blood PAI-1 and skin MMP-9 expression levels and decreases in blood adiponectin levels by UVB irradiation. In conclusion, HF diet-induced hypertrophic adipose tissue is an important cancer risk factor that promotes UV irradiation-induced carcinogenesis and tumor growth.

Ultraviolet (UV) irradiation prior to antigen immunization is employed to induce antigen-specific regulatory T cells (Tregs). UV-induced Tregs demonstrate unique bystander suppression, although antigen-specific activation is required initially. We previously reported the phenotype of alloantigen-specific transferable Tregs induced by UV-B irradiation after immunization was the same as T regulatory type 1-like CD4(+) T cells, with antigen-specific interleukin (IL)-10 production. Here, by using semi-allogeneic transplantation models in vivo, we investigated the role of IL-10 in the induction and activation of these Tregs, and the possibility of bystander suppression of third-party allograft rejection. Naïve mice (H-2(b)) were immunized with alloantigen (H-2(b/d)), and received UV-B irradiation (40 kJ/m(2)) 1 week later. Four weeks afterwards, splenic CD4(+) T cells were purified from the UV-irradiated immunized mice, and were transferred into naïve mice (H-2(b)). Allografts expressing the same alloantigen as T-cell donors were immunized against (H-2(b/d)) or an irrelevant alloantigen (H-2(b/k)) were transplanted to CD4(+) T-cell-transferred mice, and an alloantigen-specific prolongation of allograft survival observed. Experiments where IL-10 was neutralized by monoclonal antibody in the induction or effector phase revealed that IL-10 is critical, not only for induction but also for immunosuppressive function of CD4(+) Tregs induced by UV irradiation after alloantigen immunization. Third-party allografts (H-2(d/k)) were transplanted to CD4(+) T-cell-transferred mice, and graft survival was also prolonged. Even a graft only partially compatible with immunized alloantigen worked well in vivo to activate CD4(+) Tregs induced by UV irradiation after alloantigen immunization, which resulted in the bystander suppression of third-party allograft rejection.

Exposure of skin to UV radiation (UVR) prior to allergen exposure can inhibit inflammatory airways disease in mice by reducing effector CD4+ T cells in both the trachea and the airway draining lymph nodes. This study analysed the immunomodulatory properties of UVR delivered to naïve versus allergen pre-sensitised mice. In a model of inflammatory airways disease, BALB/c mice were sensitised by peritoneal injection of the allergen, ovalbumin (OVA) (20 μg/mouse), in the adjuvant, alum (4 mg/mouse), on days 0 and 14. On day 21, the mice were exposed to aerosolised OVA and 24 h later, proliferative responses by the cells in the airway draining lymph nodes were examined. UVR (8 kJ m(-2)) was administered 3 days prior to first OVA sensitisation (day -3), or OVA aerosol challenge (day 18). UVR before sensitisation reduced immune responses associated with expression of allergic airways disease; seven days after first OVA sensitisation, regulation of OVA-induced proliferation in vitro but not in vivo by CD4+CD25+ cells from UV-irradiated mice was detected. UVR administered to pre-sensitised mice regulated allergen responsiveness by cells from the airway draining lymph nodes only with a sensitisation protocol involving allergen and adjuvant at 5% strength of the original dose (1 μg OVA in 0.2 mg alum/mouse). These results suggest that UVR may modulate allergic airways disease by two mechanisms. The first, and more potent, is by reducing effector cells in respiratory tissues and requires UV delivery prior to sensitisation. The second, associated with administration to pre-sensitised mice, is weaker and is detected when the mice are sensitised with lower levels of allergen and adjuvant.

Depletion of the stratospheric ozone layer has led to increased solar UV-B radiation (280-315 nm) at the surface of the Earth. This change is likely to have had an impact on human exposure to UV-B radiation with consequential detrimental and beneficial effects on health, although behavioural changes in society over the past 60 years or so with regard to sun exposure are of considerable importance. The present report concentrates on information published since our previous report in 2007. The adverse effects of UV radiation are primarily on the eye and the skin. While solar UV radiation is a recognised risk factor for some types of cataract and for pterygium, the evidence is less strong, although increasing, for ocular melanoma, and is equivocal at present for age-related macular degeneration. For the skin, the most common harmful outcome is skin cancer, including melanoma and the non-melanoma skin cancers, basal cell carcinoma and squamous cell carcinoma. The incidence of all three of these tumours has risen significantly over the past five decades, particularly in people with fair skin, and is projected to continue to increase, thus posing a significant world-wide health burden. Overexposure to the sun is the major identified environmental risk factor in skin cancer, in association with various genetic risk factors and immune effects. Suppression of some aspects of immunity follows exposure to UV radiation and the consequences of this modulation for the immune control of infectious diseases, for vaccination and for tumours, are additional concerns. In a common sun allergy (polymorphic light eruption), there is an imbalance in the immune response to UV radiation, resulting in a sun-evoked rash. The major health benefit of exposure to solar UV-B radiation is the production of vitamin D. Vitamin D plays a crucial role in bone metabolism and is also implicated in protection against a wide range of diseases. Although there is some evidence supporting protective effects for a range of internal cancers, this is not yet conclusive, but strongest for colorectal cancer, at present. A role for vitamin D in protection against several autoimmune diseases has been studied, with the most convincing results to date for multiple sclerosis. Vitamin D is starting to be assessed for its protective properties against several infectious and coronary diseases. Current methods for protecting the eye and the skin from the adverse effects of solar UV radiation are evaluated, including seeking shade, wearing protective clothing and sunglasses, and using sunscreens. Newer possibilities are considered such as creams that repair UV-induced DNA damage, and substances applied topically to the skin or eaten in the diet that protect against some of the detrimental effects of sun exposure. It is difficult to provide easily understandable public health messages regarding "safe" sun exposure, so that the positive effects of vitamin D production are balanced against the negative effects of excessive exposure. The international response to ozone depletion has included the development and deployment of replacement technologies and chemicals. To date, limited evidence suggests that substitutes for the ozone-depleting substances do not have significant effects on human health. In addition to stratospheric ozone depletion, climate change is predicted to affect human health, and potential interactions between these two parameters are considered. These include altering the risk of developing skin tumours, infectious diseases and various skin diseases, in addition to altering the efficiency by which pathogenic microorganisms are inactivated in the environment.

We previously showed that exposure to UV radiation after immunization suppresses Th1 and Th2 immune responses, leading to impaired Ab and allo-immune responses, but the impact of UV radiation after immunization on anti-tumor immune responses mediated by tumor-specific CD8(+) T cell responses remains less clear. Furthermore, the exact phenotypic and functional characteristics of regulatory T cell population responsible for the UV-induced immunosuppression still remain elusive. Using the MBL-2 lymphoma cell line engineered to express OVA as a surrogate tumor Ag, here we demonstrate that UV irradiation after tumor Ag-immunization suppresses the anti-tumor immune response in a manner dependent on the immunizing Ag. This suppression was mediated by interleukin (IL)-10 released from CD4(+) CD25(+) T cells, by which impaired the induction of cytotoxic T lymphocytes (CTL) able to kill Ag-expressing tumor cells. In addition, we generated a panel of T cell clones from UV-irradiated and non-irradiated mice, and all of the clones derived from UV-irradiated mice had a Tr1-type regulatory T cell phenotype with expression of IL-10 and c-Maf, but not Foxp3. These Tr1-type regulatory T cell clones suppressed tumor rejection in vivo as well as Th cell activation in vitro in an IL-10 dependent manner. Given that suppression of Ag-specific CTL responses can be induced in Ag-sensitized mice by UV irradiation, our results may imply that exposure to UV radiation during premalignant stage induces tumor-Ag specific Tr1 cells that mediate tumor-Ag specific immune suppression resulting in the promotion of tumor progression.