Akademik Veri Yönetim Sistemi
INTERNATIONAL RESEARCH AND REVIEWS IN HEALTH SCIENCES, PROF. DR. HASAN AKGÜL PROF. DR. ZELIHA SELAMOĞLU, Editör, Serüven Yayınevi, Ankara, ss.202-214, 2023
Psoriasis is one of the most extensively studied chronic inflammatory skin diseases. There is not a significant hypothesis describing the unique mechanisms that elucidate the particular typical features of psoriasis. Conversely, the fluctuating behavior of psoriasis, with its remission and relapse phases, might be suggestive of its association with existing regulatory and effector immune mechanisms. Additionally, while the fact that activated T cells are crucial for the development and persistence of psoriatic lesions is undisputed, the pathophysiology of the disease can only be partly explained by the roles of keratinocytes and T lymphocytes. Other resident skin cells, including keratinocytes and dendritic cells, contribute to the development of psoriatic plaques. This cellular contribution is associated with strong and dynamic epigenetic effects. Various studies have indicated that structural defects in keratinocytes are fundamental to the development of psoriasis. A growing number of specific target molecules found in genes controlling proliferation and differentiation processes in the epidermis as well as T cell recruitment and keratinocyte inflammatory activation have been associated with the disease. In the current review, we covered research on the pathophysiology of psoriasis within the framework of signaling between keratinocytes and immune cells. Our aim is to delineate how disordered immune responses that contribute to the development of psoriatic plaques and inflammation emerge from the axis of keratinocyte-immune cell interactions. Despite the precise sequence of events that leads to the formation of psoriatic plaques and the cytokine cascade remaining unknown, identifying early triggers and the roles of keratinocytes and T cells might provide novel, promising targets for the prevention and effective treatment of psoriasis.