Background: Continual surveillance based on patch test results has proved useful for the identification of contact allergy.Objectives: To provide a current view on the spectrum of contact allergy to important sensitizers across Europe.Patients/Methods: Clinical and patch test data of 19 793 patients patch tested in 2005/2006 in the 31 participating departments from 10 European countries (the European Surveillance System on Contact Allergies' (ESSCA) www.essca‐dc.org) were descriptively analysed, aggregated to four European regions.Results: Nickel sulfate remains the most common allergen with standardized prevalences ranging from 19.7% (central Europe) to 24.4% (southern Europe). While a number of allergens shows limited variation across the four regions, such as Myroxylon pereirae (5.3–6.8%), cobalt chloride (6.2–8.8%) or thiuram mix (1.7–2.4%), the differences observed with other allergens may hint on underlying differences in exposures, for example: dichromate 2.4% in the UK (west) versus 4.5–5.9% in the remaining EU regions, methylchloroisothiazolinone/methylisothiazolinone 4.1% in the South versus 2.1–2.7% in the remaining regions.Conclusions: Notwithstanding residual methodological variation (affecting at least some ‘difficult’ allergens) tackled by ongoing efforts for standardization, a comparative analysis as presented provides (i) a broad overview on contact allergy frequencies and (ii) interesting starting points for further, in‐depth investigation.

Natural killer T (NKT) cells are a unique subset of lymphocytes that express NK cell markers such as CD161 and CD94, as well as a T-cell receptor (TCR) α/β, with a restricted repertoire, which distinguishes them from NK cells, which lack a TCR. In contrast to conventional T-lymphocytes, the TCR of NKT cells does not interact with that of peptide antigens presented by classical major histocompatibility complex-encoded class I or II molecules. Instead, this TCR recognizes glycolipids presented by CD1d, a non-classical antigen-presenting molecule. The rapid response of NKT cells to their cognate antigens is characteristic of an innate immune response, and allows the polarizing cytokines (IFN-γ and/or IL-4) to regulate adaptive immunity. NKT cells have been found to be critical in the immune response against viral infections and malaria, as well as in tumor immunity, and certain autoimmune diseases. NKT cells have been assessed to represent the “trait d’union” between innate and adaptive immunity. They play an active role in skin diseases, such as contact sensitivity, which have been implicated in UV-induced immunosuppression and psoriasis. Thus, NKT-cells are emerging as an important subset of lymphocytes, with a protective role in host defense and a pathogenic role in certain immune-mediated disease states.

Doxycycline is used to treat infective diseases because of its broadspectrum efficacy. High dose administration (100 or 200 mg/day) is often responsible for development of bacterial resistances and endogenous flora alterations, whereas low doses (20–40 mg/day) do not alter bacteria susceptibility to antibiotics and exert anti‐inflammatory activities. In this study, we wanted to assess the efficacy of both low and high doxycycline doses in modulating IL‐8, TNF‐α, and IL‐6 gene expression in HaCaT cells stimulated with LPS. Three experimental settings were used, differing in the timing of doxycycline treatment in respect to the insult induced by LPS: pretreatment, concomitant, and posttreatment. Low doses were more effective than high doses in modulating gene expression of LPS‐induced proinflammatory cytokines (IL‐8, TNF‐α, and IL‐6), when added before (pretreatment) or after (posttreatment) LPS stimulation. This effect was not appreciated when LPS and doxycycline were simultaneously added to cell cultures: in this case high doses were more effective. In conclusion, our in vitro study suggests that low doxycycline doses could be safely used in chronic or acute skin diseases in which the inflammatory process, either constantly in progress or periodically recurring, has to be prevented or controlled.

IL‐33 is a novel pro‐inflammatory cytokine and ligand for the orphan receptor ST2. Although originally defined as an inducer of Th2‐mediated responses, IL‐33 was recently found to be involved in arthritis, a Th1/Th17‐mediated disease. Here, we assessed the ability of IL‐33 to promote inflammation via mast cells (MCs) and keratinocytes (KCs) activation in psoriasis. IL‐33 resulted elevated in the skin but not in the serum of psoriasis patients. IL‐33 was secreted by psoriasis KCs and HaCaT cells after TNF‐α stimulation. In HMC‐1, TNF‐α, but not IL‐17, could induce a robust increase in IL‐33 expression. In HaCaT cells, TNF‐α was able to induce IL‐6, MCP‐1 and VEGF, and the addition of IL‐33 reinforced these increases. TNF‐α + IL‐33 combination showed similar results in primary KCs and ex vivo skin organ culture. In conclusion, our study suggests that IL‐33 may be involved in psoriasis biology via MCs and KCs.