Topically Delivered Tumor Necrosis Factor-α–Targeted Gene Regulation for PsoriasisPsoriasis is a highly visible, chronic, immune-mediated inflammatory skin disorder that affects 2–3% of the US population (Lowes et al., 2014). Tumor necrosis factor-α (TNF-α) and IL-17A synergistically up-regulate the production of other cytokines, chemokines, and antimicrobial peptides from keratinocytes and regional immune cells, initiating and perpetuating the immune activation of psoriasis (Chiricozzi et al., 2011; Di Cesare et al., 2009; Ettehadi et al., 1994; Harden et al., 2015; Lowes et al., 2005).
Recent Highlights in Psoriasis ResearchThis article highlights recent advances in the immunology, epidemiology, and genetics/genomics of psoriasis. Advances sometimes generate more questions, and this article makes an attempt to point out where controversies might exist in the literature. Many of the articles mentioned were published in the Journal of Investigative Dermatology, but many articles from the broader scientific literature are also cited, to provide context and to add further validity for some of these key findings. Among the themes we explore are the identification of antigens in psoriasis, the co-morbidities of psoriasis, and novel integrative approaches to genome-wide association studies.
microRNAs in PsoriasisPsoriasis is a chronic inflammatory skin condition resulting from a complex interplay among the immune system, keratinocytes, susceptibility genes, and environmental factors. However, the pathogenesis of psoriasis is not completely elucidated. microRNAs represent a promising class of small, noncoding RNA molecules that function to regulate gene expression. Although microRNA research in psoriasis and dermatology is still relatively new, evidence is rapidly accumulating for the role of microRNAs in the pathogenesis of psoriasis and other chronic inflammatory conditions.