Plaque-based sub-blistering dosimetry: Reaching PASI-75 after two treatments with 308-nm excimer laser in a generalized psoriasis patient.

BACKGROUND: Generalized UVB phototherapy has been established as an effective and safe treatment for chronic plaque-type psoriasis for decades and in recent years, targeted 308-nm excimer laser has emerged as an equally safe and more effective treatment option. While traditional dosimetry for laser has been determined either through minimal erythema dose (MED) or a combination of the patient's Fitzpatrick skin type and the level of plaque induration, we have developed "Plaque-based Sub-blistering Dosimtery" based on observations that administering anywhere from 8 to 16 multiples of MED to psoriatic plaques has resulted in clearance after one treatment with longer remission rates than the traditional dosing protocol. CASE REPORT: The authors describe a case in which a patient achieved PASI 75 following only two treatments with 308 nm excimer laser using this new protocol. Biopsies taken before and after treatment reveal a dramatic decrease in CD4+T cells as well as TNF-alpha- and IL-2-producing T cells. CONCLUSION: This case demonstrates using a more aggressive dosing protocol determined by plaque testing is well-tolerated and can lead to excellent clearance with minimal side effects and comorbidity.

Genetic Epidemiology of Psoriasis.

Psoriasis is a chronic, inflammatory, immune-mediated skin condition with a prevalence of 0-11.8% across the world. It is associated with a number of cardiovascular, metabolic, and autoimmune disease co-morbidities. Psoriasis is a multifactorial disorder, influenced by both genetic and environmental factors. Its genetic basis has long been established through twin studies and familial clustering. The association of psoriasis with the HLA-Cw6 allele has been shown in many studies. Recent genome-wide association studies have identified a large number of other genes associated with psoriasis. Many of these genes regulate the innate and adaptive immune system. These findings indicate that a dysregulated immune system may play a major role in the pathogenesis of psoriasis. In this article, we review the clinical and genetic epidemiology of psoriasis with a brief description of the pathogenesis of disease.

Memory regulatory T cells reside in human skin.

Regulatory T cells (Tregs), which are characterized by expression of the transcription factor Foxp3, are a dynamic and heterogeneous population of cells that control immune responses and prevent autoimmunity. We recently identified a subset of Tregs in murine skin with properties typical of memory cells and defined this population as memory Tregs (mTregs). Due to the importance of these cells in regulating tissue inflammation in mice, we analyzed this cell population in humans and found that almost all Tregs in normal skin had an activated memory phenotype. Compared with mTregs in peripheral blood, cutaneous mTregs had unique cell surface marker expression and cytokine production. In normal human skin, mTregs preferentially localized to hair follicles and were more abundant in skin with high hair density. Sequence comparison of TCRs from conventional memory T helper cells and mTregs isolated from skin revealed little homology between the two cell populations, suggesting that they recognize different antigens. Under steady-state conditions, mTregs were nonmigratory and relatively unresponsive; however, in inflamed skin from psoriasis patients, mTregs expanded, were highly proliferative, and produced low levels of IL-17. Taken together, these results identify a subset of Tregs that stably resides in human skin and suggest that these cells are qualitatively defective in inflammatory skin disease.