Psoriasis: A Comprehensive Review

S100 Proteins as Novel Therapeutic Targets in Psoriasis and Other Autoimmune Diseases

“…Psoriasis is defined as a systemic, chronic immune-mediated inflammatory disease that affects approximately 1–3% of the population worldwide [ 24 ]. It is a non-contagious, papule-exfoliative disease, affecting women and men equally [ 25 , 26 , 27 ]. Psoriasis can occur at any age, but it usually appears for the first time between 15 and 25 years of age (type I psoriasis) and after 40 years (type II psoriasis).…”

“…This disease is characterized by alternating severity and remission of disease symptoms, which include the formation of skin lesions of varying severity in the form of symmetrical, sharply delimited erythematous papules, usually covered with white, shiny scales [ 28 , 29 ]. Skin lesions in psoriasis can occupy symmetrically all areas of the body, but the most characteristic places of lesions are elbows and knees, straight surfaces of the upper and lower limbs, lumbosacral region, trunk, hands and feet, hairy scalp, skin folds, nails, and under the breasts and genitals [ 26 , 27 , 30 ]. When the scales are scraped off the surface of the lump, the scales fall off, forming thin flakes reminiscent of candle scrapings (a sign of a stearic candle) [ 25 ].…”

“…Punctate bleeding spots are also evident, which is called the Auspitz’s sign [ 30 ]. The clinical manifestations of psoriasis vary considerably from patient to patient ( Figure 1 ), from individual eruptions to generalized lesions, and the lack of a biological marker of disease makes it difficult to diagnose [ 25 , 26 , 27 , 30 , 31 ]. For this reason, different morphological forms of psoriasis are distinguished.…”

“…Both DNA synthesis and mitotic activity are increased. It is thought that these changes stem from the premature maturation of keratinocytes induced by the activation of immune cells and the beginning inflammatory cascade in the dermis [ 27 , 32 ]. During psoriasis, abnormal infiltrating of T-cells, dendritic cells (DCs), macrophages, and neutrophils into the skin are observed [ 31 ].…”

“…One hypothesis assumes the activation of DCs through recognition of AMPs. Dying cells release DNA, which, together with antimicrobial proteins produced by keratinocytes and infiltrating immune cells, form complexes that may act as an inflammatory stimulus by stimulating receptors on plasmacytoid DCs that in turn produce the cytokine IFN-α [ 27 ]. IFN-α then triggers activation, maturation, and differentiation of conventional DCs, which may stimulate T-cells through IL-23.…”