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Skin cancer is the most common type of cancer in the US with an increasing prevalence worldwide. While ultraviolet (UV) radiation is a well-known risk factor, there is emerging evidence that the microbiota may also contribute. In recent years, the human microbiota has become a topic of great interest, and its association with inflammatory skin diseases (i.e., atopic dermatitis, acne, rosacea) has been explored. Little is known of the role of microbiota in skin cancer, but with the recognized link between microbial dysbiosis and inflammation, and knowledge that microbiota modulates the effect of UV-induced immunosuppression, theories connecting the two have surfaced. In this paper, we provide a comprehensive review of the key literature on human microbiota, especially the skin microbiota, and skin cancer (i.e., non-melanoma skin cancer, melanoma, cutaneous T cell lymphoma). Also, mechanistic perspectives as to how our microbiota influence skin cancer development and treatment are offered. [ABSTRACT FROM AUTHOR]

Psoriasis is a recurrent, chronic, immune-mediated, systemic inflammatory disease of the skin, joints, and other organic systems. After atopic dermatitis, chronic stationary psoriasis is the most common inflammatory skin disease, affecting an average of 2–4% of the world's population. The disease carries a significant burden due to its numerous comorbidities and the major impact on patients' social and emotional aspects of life. According to current knowledge, psoriasis is a multifactorial disease that occurs in genetically predisposed individuals under various environmental factors, which trigger an immune response disorder with a series of complex inflammatory cascades. The disease is initiated and maintained by mutual interaction of the innate and adaptive immune cells, primarily dendritic cells, T lymphocytes, and keratinocytes, whose leading role alternates at different stages of the disease, consisting mainly in the IL-23/Th17 pathway. Inflammatory events result in consequent epidermal and dermal changes and evolution of the characteristic psoriatic phenotype, respectively. This paper aims to present a comprehensive overview of current knowledge on psoriasis genetic and environmental etiological factors, immunopathogenesis, and the leading cellular and cytokine participants in the inflammatory pathways of this disease. [ABSTRACT FROM AUTHOR]

Background Variable results have been obtained when patients with atopic dermatitis (AD),) have been patch tested with allergens known to produce a positive prick lest. The significance of patch test results in our understanding of the pathogenesis of AD therefore remains questionable. Objective This study was designed to determine the relevance of either positive or negative patch test results in relation to the expression of cell mediated immunity to allergens in patients with AD. Methods Thirty-five patients with AD exhibiting patch test positivity to one or more aeroallergens on "tape stripped* areas of the back were retested without prior tape stripping. Nine patients again showed positivity to one or more allergens while 26 failed to show positive reactions. In six of the positive patients both positive and negative patch tests were observed. Skin biopsies were taken from these matched positive and negative patch test sites as well as from an area of uninvolved skin. Samples were frozen and cryostat sections were analysed with immunohistological techniques using monoclonal antibodies to investigate the distribution of immunocompetent cells. Results All positive patch tests exhibited characteristics of a cell mediated immune response. The negative patch test sites were also found to contain evidence of mononuclear cell infiltration. Both negative and positive patch test sites showed significantly greater proportions of T cells compared to uninvolved skin. No increase in numbers of RFDl positive and RFD7 positive macrophages were observed in either positive or negative patch test sites. Expression of CD23 by CDl positive Langerhans cells was raised in both negative and positive patch tests compared to uninvolved areas. A significant increase in the population (RFD7+, CD23+) was seen in positive patch test sites compared to uninvolved skin. An increase in the proportion of RFDl positive cells expressing CD23 was also seen in both negative and positive patch tests compared to uninvolved skin. Conclusions This paper demonstrates that immunological reactions are promoted at 'non-tape stripped' patch test sites where no clinical evidence of reactivity is seen. Together the data demonstrate that the presence of systemic cell mediated immunity to specific allergens identified in patients by positive patch test, may also be present when no clinical signs are seen at the patch test site. [ABSTRACT FROM AUTHOR]