THE ROLE OF LOCAL INFLAMMATION IN THE IMMUNOPATHOGENESIS OF PSORIASIS

Psoriasis is one of the most prevalent chronic recurrent multifactorial diseases of the skin with a predominance of a genetic factor characterized by hyperproliferation of epidermal cells, the keratinisation impairment against the background of inflammatory reactions in the dermis, as well as lesions of the nails, joints and scalp, provoked by exogenous and endogenous factors. This disease can also be characterized by erythema, scaly elements, papules and plaques. According to the results of clinical and epidemiological research, about 3 – 4% of the population worldwide is diagnosed to have psoriasis, regardless of gender, age and ethnic group. The share of this pathology in the overall structure of skin diseases reaches from 1% - to 40%, according to various authors. They consider psoriasis as a systemic disease involving not only the skin, but also joints and viscera, and call it as a “psoriasis disease”. The causes of psoriasis are immunological disorders and genetic defects. Recently inflammation in the skin of psoriasis patients is considered as an autoimmune process, in which a key role is played by T-cells sensitized to keratinocytes. One of the most probable self-antigens that trigger an immune inflammation in psoriasis may be cytosolic DNA. We describe the functions of the subpopulations of immune cells and the effects of secreted cytokines in the pathogenesis of psoriasis: the dendritic cells — Langerhans cells, plasmacytoid dendritic cells, CD11c+ dendritic cells; T-cells — T helper type 1 and 17, cytotoxic T lymphocytes, T-regulatory lymphocytes. The development of T-cell memory and intradermal proliferation of T-cells in the skin of patients plays an important role in the development of relapses of psoriasis. Therefore, the goal of further research is to carry out more in-depth study of the immunopathogenesis of psoriatic disease that will reveal new targets for the treatment of this dermatosis.