CD4+ T Cells and S100A7 Epression in Normal and Psoriatic Skin: A Histological and Histochemical Study
CD4+ T Cells and S100A7 Epression in Normal and Psoriatic Skin: A Histological and Histochemical Study
Psoriasis is one of the commonest and most researched chronic immune-mediated inflammatory skin disorders that affects approximately 1-3% of the population worldwide and significantly impairs patients' quality of life. The most common form is plaque psoriasis, which makes up about 90% of cases, which primarily manifests as sharply demarcated, erythematous, scaly plaques, which can involve any part of the skin but most commonly the extensor surfaces (such as the elbows and knees) and the scalp. Apart from plaque psoriasis, there are also other clinical forms, such as guttate psoriasis (particularly common in children after strep throat infections), and pustular psoriasis (one of the most severe varieties of psoriasis, in which the spreading of pustules is generalized, with epidermal fulfillment and a severe general condition).
This disease is characterized by alternating severity and remission of disease symptoms, which include the formation of skin lesions of varying severity. The psoriasis area and severity index (PASI) is a widely used instrument in psoriasis trials that assesses and grades the severity of psoriatic lesions and the patient's response to treatment. It produces a numeric score ranging from 0 to 72. In general, a score of 5 to 10 is considered moderate disease, and a score over 10 is considered severe.
A series of basic and clinical studies have shown that psoriasis is mediated by components of both the innate and adaptive immune systems. The crosstalk between keratinocytes and various immune cells, especially helper T cells, plays a central role in the progression of psoriasis. Psoriasis is caused by chronic interaction between keratinocytes and activated immune cells. Numerous studies have established that hyperproliferation and abnormal differentiation of keratinocytes is a secondary phenomenon induced by immune activation. This "immune" hypothesis, is mainly based on dendritic cell (DC) and T cell pathogenic functions.The abnormal expression of S100A7 as a part of innate immunity in psoriasis vulgaris has been confirmed. S100 proteins are being discussed not only as potential biomarkers as well as new therapeutic targets through inhibition of S100 protein expression, targeted degradation, and antibody-mediated binding of S100 proteins. The most common therapeutic approaches include inhibition of S100 protein expression using microRNA-, small interfering RNA- or short hairpin RNA-based knockdown of S100 proteins using neutralizing antibodies or using specific small-molecule inhibitors. On the other side the role of CD4+ T cells (Th 17 cells) as a part of adaptive immunity, seems to be critical in the development of the skin lesions. Whether S100A7 or Th 17 cells are related to the severity of psoriasis is unclear. Immunohistology provides invaluable tools for better understanding psoriasis's pathogenetic mechanism and understanding the molecular processes involved in the pathogenesis of psoriasis.
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