Psoriasis is one of the most common immune-mediated chronic, inflammatory skin diseases characterized by hyperproliferative keratinocytes and infiltration of T cells, dendritic cells, macrophages and neutrophils. Although the pathogenesis of psoriasis is not fully understood, there is ample evidence suggesting that the dysregulation of immune cells in the skin, particularly T cells, plays a critical role in psoriasis development. In this review, we mainly focus on the pathogenic T cells and discuss how these T cells are activated and involved in the disease pathogenesis. Newly identified 'professional' IL-17-producing dermal cd T cells and their potential role in psoriasis will also be included. Finally, we will briefly summarize the recent progress on the T cell and its related cytokine-targeted therapy for psoriasis treatment.

Dermal IL-17-producing γδT cells play a critical role in skin inflammation. However, their development and peripheral regulation have not been fully elucidated. Here we demonstrate that dermal γδT cells develop from the embryonic thymus and undergo homeostatic proliferation after birth with diversified TCR repertoire. Vγ6T cells are bona fide resident but precursors of dermal Vγ4T cells may require extrathymic environment for imprinting skin homing properties. Thymic Vγ6T cells are more competitive than Vγ4 for dermal γδT cell reconstitution and TCRδ−/− mice reconstituted with Vγ6 develop psoriasis-like inflammation after IMQ-application. Although both IL-23 and IL-1β promote Vγ4 and Vγ6 proliferation, Vγ4 are the main source of IL-17 production, which requires IL-1 signaling. Mice with deficiency of IL-1RI signaling have significantly decreased skin inflammation. These studies reveal a differential developmental requirement and peripheral regulation for dermal Vγ6 and Vγ4 γδT cells, implying a new mechanism that may be involved in skin inflammation.

The IL-1 signaling pathway has been shown to play a critical role in the pathogenesis of chronic, autoinflammatory skin diseases such as psoriasis. However, the exact cellular and molecular mechanisms have not been fully understood. Here, we show that IL-1β is significantly elevated in psoriatic lesional skin and imiquimod-treated mouse skin. In addition, IL-1R signaling appears to correlate with psoriasis disease progression and treatment response. IL-1 signaling in both dermal γδ T cells and other cells such as keratinocytes is essential to an IMQ-induced skin inflammation. IL-1β induces dermal γδ T cell proliferation and IL-17 production in mice. In addition, IL-1β stimulates keratinocytes to secrete chemokines that preferentially chemoattract peripheral CD27 CCR6IL-17 capable of producing γδ T cells (γδT17). Further studies showed that endogenous IL-1β secretion is regulated by skin commensals to maintain dermal γδT17 homeostasis in mice. Mouse skin associated with Corynebacterium species, bacteria enriched in human psoriatic lesional skin, has increased IL-1β and dermal γδT17 cell expansion. Thus, the IL-1β-IL-1R signaling pathway may contribute to skin inflammation and psoriasis pathogenesis via the direct regulation of dermal IL-17-producing cells and stimulation of keratinocytes for amplifying inflammatory cascade.

Environmental economists have long used surveys to gather information about people's preferences. A recent innovation in survey methodology has been the advent of web-based surveys. While the Internet appears to offer a promising alternative to conventional survey administration modes, concerns exist over potential sampling biases associated with web-based surveys and the effect these may have on valuation estimates. This paper compares results obtained from a travel cost questionnaire of visitors to Fraser Island, Australia, that was conducted using two alternate survey administration modes; conventional mail and web-based. It is found that response rates and the socio-demographic make-up of respondents to the two survey modes are not statistically different. Moreover, both modes yield similar consumer surplus estimates.

This paper examines the influence of public greenspace on the life satisfaction of residents of Australia's capital cities. A positive relationship is found between the percentage of public greenspace in a resident's local area and their self-reported life satisfaction. On average, it is found that a resident has an implicit willingness-to-pay of $1,168 in annual household income for a one per cent (143m 2) increase in public greenspace. The relationship between public greenspace and life satisfaction however, is non-linear. Additional results suggest that the value of greenspace increases with population density and that lone parents, the less educated and those living in high rise dwellings benefit to a greater extent from the provision of public greenspace than the general population. In all, life satisfaction data supports existing evidence that public greenspace is welfare enhancing for urban residents and adequate allowance should be made for its provision when planning urban areas.