Evaluation of the effect of NB-UVB phototherapy on HMGB1 expression in chronic plaque type psoriasis

Abstract

Psoriasis affects nearly 2-3% of the world's population. Its profound effect on the patients’ quality of life as well as its associated co-morbidities caused it to be one of the most studied dermatological diseases. Psoriasis is a chronic inflammatory skin disease characterized by hyper proliferation of keratinocytes, dilation and growth of dermal capillary vasculture, and cellular infiltrate of activated T cells, dendritic cells, monocytes, and neutrophils. Increased production of numerous cytokines, chemokines and growth factor has been found to be present within the skin as well as in the circulation in psoriasis patients. Nowadays, it is believed that psoriasis is most likely a Th1/Th17 induced inflammatory disease, with interplay between genetic susceptibility, defects in skin barrier and dysregulation of innate and adaptive immunity. Environmental factors also play a role in the pathogenesis of psoriasis including drugs, skin trauma, infection and stress. High mobility group box-1 (HMGB1), initially described as a non histone nuclear protein with transcriptional regulatory properties, is now recognized as a late mediator in septic shock as well as a pro- inflammatory cytokines. HMGB1 is expressed by almost all cells, and usually located in the nucleus. However, it has been reported that HMGB1 can be translocated to the cytosol and then released into the extracellular space. There are two pathways in which HMGB1 can be released extracellularly. One is an active process which occurs when cells exposed to inflammatory mediators, such as lipopolysaccharide (LPS), (TNF)- α, and (IFN)-γ ; the other a passive process during cellular necrosis.