Psoriasis is a common chronic immune-mediated inflammatory skin disorder, affecting the skin, nails, and joints in both children and adults. Depending on the studied population, psoriasis is estimated to affect 2.0–8.5% of the population [1]. The main causes of psoriasis remain unknown, although a complex of interactions between genetic, biochemical, and immunological abnormalities have been involved [1]. Regarding the genetic aspects, PSORS1 (at chromosome 6p21) is the major susceptibility locus for psoriasis [1–3]. Many HLA markers have been associated with psoriasis, but HLA-Cw6 is the highest relative risk for psoriasis in Caucasian population. However, as reported above, the onset of a psoriatic lesion is a complex and multicellular process that involves keratinocytes, T cells (above all CD4+ T cells in the upper dermis and CD8+ T cells in the epidermis), dendritic cells, macrophages, mast cells, endothelial cells, and neutrophils. While, at the same time, cytokines (e.g., TNF-alpha, IL-17, IL-23, etc.) and growth factor initiate and sustain inflammation in this process [1]. The cutaneous microbiota of patients with psoriasis is different to those without psoriasis, although the significance of this is unclear [4]. Indeed a wide range of microorganisms have been associated with psoriasis; however, the microorganism that is most associated with the onset of psoriasis is Streptococcus. Indeed, in some cases, psoriatic patients show a higher incidence of Beta-hemolytic streptococci of Lancefield groups A, C, and G, exacerbating the cutaneous symptomatology [5]. In this regard, Th1 cells recognize bacteria of the class of A streptococci and a HLA variation shows a specific effect on the immune response to group A streptococci [5]. Finally, also some drugs can induce the onset of psoriasis in some predisposed subjects, such as beta-blockers, lithium, antimalarials, terbinafine, calcium channel blockers, captopril, glyburide, granulocyte colony-stimulating factor, interleukins and interferons [5]. Finally, various studies highlighted a correlation between stress and severity of psoriasis, where stress seems to play a pivotal role for the onset and/or exacerbation of psoriasis [5].

Psoriasis in Adolescents and Adults / Mercuri, S. R.; Paolino, G.; Longhi, E. V.. - (2023), pp. 105-114. [10.1007/978-3-031-31307-3_10]

Psoriasis in Adolescents and Adults

Mercuri S. R.
Primo
;
Paolino G.
Secondo
;
2023-01-01

Abstract

Psoriasis is a common chronic immune-mediated inflammatory skin disorder, affecting the skin, nails, and joints in both children and adults. Depending on the studied population, psoriasis is estimated to affect 2.0–8.5% of the population [1]. The main causes of psoriasis remain unknown, although a complex of interactions between genetic, biochemical, and immunological abnormalities have been involved [1]. Regarding the genetic aspects, PSORS1 (at chromosome 6p21) is the major susceptibility locus for psoriasis [1–3]. Many HLA markers have been associated with psoriasis, but HLA-Cw6 is the highest relative risk for psoriasis in Caucasian population. However, as reported above, the onset of a psoriatic lesion is a complex and multicellular process that involves keratinocytes, T cells (above all CD4+ T cells in the upper dermis and CD8+ T cells in the epidermis), dendritic cells, macrophages, mast cells, endothelial cells, and neutrophils. While, at the same time, cytokines (e.g., TNF-alpha, IL-17, IL-23, etc.) and growth factor initiate and sustain inflammation in this process [1]. The cutaneous microbiota of patients with psoriasis is different to those without psoriasis, although the significance of this is unclear [4]. Indeed a wide range of microorganisms have been associated with psoriasis; however, the microorganism that is most associated with the onset of psoriasis is Streptococcus. Indeed, in some cases, psoriatic patients show a higher incidence of Beta-hemolytic streptococci of Lancefield groups A, C, and G, exacerbating the cutaneous symptomatology [5]. In this regard, Th1 cells recognize bacteria of the class of A streptococci and a HLA variation shows a specific effect on the immune response to group A streptococci [5]. Finally, also some drugs can induce the onset of psoriasis in some predisposed subjects, such as beta-blockers, lithium, antimalarials, terbinafine, calcium channel blockers, captopril, glyburide, granulocyte colony-stimulating factor, interleukins and interferons [5]. Finally, various studies highlighted a correlation between stress and severity of psoriasis, where stress seems to play a pivotal role for the onset and/or exacerbation of psoriasis [5].
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.11768/184908
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