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NCT Number: NCT06050330

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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Key information

Sex eligibility

All sexes

Study type

Interventional

Phase

Not applicable

Primary location

Sohag university Hospital

Sohag, Egypt

Who can participate

Healthy volunteers accepted: No

Only the study team can determine whether someone qualifies for participation.

Inclusion criteria

  • the study will include patients with psoriasis

Exclusion criteria

  • pregnancy
  • lactation

Treatment and study plan

Skin Biopsy

Diagnostic Test

Paraffin sections,5 Um thick will be prepared from the skin samples and will be analyzed for light microscopy

Primary outcomes

  1. immunohistochemical skin expression of S100A7 (psoriasin)

    Time frame: 1 year

    measuring the percentage area of S100A7 (psoriasin) positive cells in skin by immunohistochemistry

  2. immunohistochemical skin expression of CD4 T cells

    Time frame: 1 year

    measuring number of CD4 T positive cells in skin by immunohistochemistry

Sponsors and collaborators

Lead sponsor

Sohag University

Other

Registry information

Important dates

Study start
2023
Primary completion
2024
Study completion
2024
First posted
Sep 22, 2023
Registry last updated
Jan 23, 2026

OpenTrials presents study information sourced from ClinicalTrials.gov. The official registry record should be consulted for the latest information.

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This listing is for discovery and informational purposes only. It is not medical advice, does not guarantee that a study is recruiting, and does not determine eligibility. Contact the study team and a qualified healthcare professional when considering participation.

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