Marijana Vičić

Cytotoxic T lymphocytes as a potential brake of keratinocyte proliferation in psoriasis

Psoriasis is a chronic papulosquamous skin disease, histologically characterized by epidermal hyperproliferation and dermal infiltration of inflammatory cells. The majority of T lymphocytes infiltrating dermis are CD4+ T lymphocytes secreting type 1 and type 17 cytokines. These cytokines are responsible for triggering keratinocyte proliferation as well as chemokine secretion and subsequent migration of other inflammatory cells in the skin. Contrarily, lymphocytes that accumulate in epidermis are mainly CD8+ T lymphocytes. According to the recent findings, these cells can also secrete type 1 and type 17 cytokines. However, it is demonstrated so far that epidermal CD8+ T lymphocytes contain higher amounts of cytolytic molecules, such as perforin, granzyme B and granulysin whose role in psoriasis pathogenesis is still unknown. Therefore, in this article we hypothesize the active involvement of cell mediated cytotoxicity in killing the proliferating keratinocytes as a mechanism of potential self-defense and possible brake in psoriatic plaque formation, maintaining skin homeostasis.

Human Hair Follicle: An Update on Biology and Perspectives in Hair Growth Disorders Treatment

The Hair Follicle (HF) is a vital component of mammalian skin and represents a unique, highly regenerative system that undergoes phases of rapid growth, regression, and resting periods. The hair cycling is of profound clinical relevance since majority of the hair growth disorders occur as a result of cycle changes. The influence of many molecules governing the formation of HF has been investigated and many of important cycle mediators have been identified. Cellular and molecular events during cycling are controlled by a network of sequential activation of autocrine, paracrine and endocrine signaling pathways. This implies variations in the expression or activity of the Wnt family molecules, Fibroblast Growth Factor (FGF), Transforming Growth Factor β (TGF-β), Hedgehog pathway, β-Catenin pathway, noggin, transcription factor Stat3, Epidermal Growth Factor (EGF), Insulin Growth Factor-1 (IGF- 1), Vascular Endothelial Growth Factor (VEGF), Thyrotropin Releasing Hormone (TRH), Polyamine, Spermidine, Neurotrophins (NT3, NT4), prolactin, retinoids, Bone Morphogenetic Protein 4 (BMP4), cathepsin L, 17-β estradiol, dihydrotestosterone and many others. Despite considerable progress in this area, the key elements of cycle control have not been identified. Therefore, for the most common hair disorders several agents are available, even none of these is curative or preventive. The one of the prime challenges of hair research is a better understanding of the molecular controls of hair cycling and developing drug which would effectively manipulate the cycle. Future therapy strategies will be based on new and better knowledge about the HF biology. Until than, alopecia areata, telogen effluvium and androgenetic alopecia, will remain unsolved medical problems.