LANGERHANS CELLS AND GAMMA DELTA LYMPHOCYTES IN THE PATHOGENESIS OF PSORIASIS

Abstract

Psoriasis is a frequently occurring inflammatory skin disease. Fundamental research into the pathogenesis of psoriasis has significantly expanded our understanding of skin immunology, which has enabled the introduction of innovative and highly effective therapies. Psoriasis is a largely T-lymphocyte-mediated disease in which activation of innate immune cells and pathogenic T cells leads to inflammation and hyperproliferation of keratinocytes. Langerhans cells (LCs) like dendritic cells (DCs), which play an important role in the immune system, are mainly distributed in the epidermis. Since human and mouse skin DC subpopulations share common ontogenetic characteristics, we can further investigate the role of DCs in psoriatic inflammation in mice. T cells are an unconventional population of T lymphocytes that play an indispensable role in host defense, immune surveillance, and immune system homeostasis. Although T cells constitute only a small fraction of the total T cell pool, emerging evidence suggests that aberrantly activated T cells may play a role in the pathogenesis of psoriasis. Dermal T cells are the major IL-17-producing cells in the skin that respond to IL-23 stimulation. In addition, T cells have characteristics of memory cells that mediate repeated episodes of psoriatic inflammation. This review discusses the mechanisms by which Langerhans cells and T cells participate in the pathogenesis of psoriasis.