CD4+ T Cells and S100A7 Epression in Normal and Psoriatic Skin: A Histological and Histochemical Study

NCT06050330 | Completed

• 1 other identifier: soh-Med-23-09-01MS
• Study Type: interventional
• Target: 40
• Locations: 1 country
• Sites: 1

Brief Summary

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.

Conditions

Psoriasis

Outcome Measures

Primary Outcomes (2)

• immunohistochemical skin expression of S100A7 (psoriasin)

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

  1 year

• immunohistochemical skin expression of CD4 T cells

  measuring number of CD4 T positive cells in skin by immunohistochemistry

  1 year

Study Arms (2)

cases group

ACTIVE COMPARATOR

patients with psoriasis

Diagnostic Test: skin biopsy

control group

ACTIVE COMPARATOR

Healthy

Diagnostic Test: skin biopsy

Interventions

skin biopsy DIAGNOSTIC_TEST

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

cases group; control group

Eligibility Criteria

• Sex: all
• Healthy Volunteers: No
• Age Groups: Child (0-17), Adult (18-64), Older Adult (65+)

You may qualify if:

• the study will include patients with psoriasis

You may not qualify if:

• pregnancy
• lactation

Sponsors & Collaborators

• Sohag University: lead

Study Sites (1)

Sohag university Hospital

Sohag, Egypt

Location

Related Publications (4)

• Iskandar IYK, Parisi R, Griffiths CEM, Ashcroft DM; Global Psoriasis Atlas. Systematic review examining changes over time and variation in the incidence and prevalence of psoriasis by age and gender. Br J Dermatol. 2021 Feb;184(2):243-258. doi: 10.1111/bjd.19169. Epub 2020 Jun 21.

  PMID: 32358790 BACKGROUND

• Lowes MA, Suarez-Farinas M, Krueger JG. Immunology of psoriasis. Annu Rev Immunol. 2014;32:227-55. doi: 10.1146/annurev-immunol-032713-120225.

  PMID: 24655295 BACKGROUND

• Yadav K, Singh D, Singh MR. Protein biomarker for psoriasis: A systematic review on their role in the pathomechanism, diagnosis, potential targets and treatment of psoriasis. Int J Biol Macromol. 2018 Oct 15;118(Pt B):1796-1810. doi: 10.1016/j.ijbiomac.2018.07.021. Epub 2018 Jul 11.

  PMID: 30017989 BACKGROUND

• Michalek IM, Loring B, John SM. A systematic review of worldwide epidemiology of psoriasis. J Eur Acad Dermatol Venereol. 2017 Feb;31(2):205-212. doi: 10.1111/jdv.13854. Epub 2016 Aug 30.

  PMID: 27573025 BACKGROUND

MeSH Terms

Conditions

Psoriasis

Condition Hierarchy (Ancestors)

Skin Diseases, Papulosquamous; Skin Diseases; Skin and Connective Tissue Diseases

Study Design

• Study Type: interventional
• Phase: not applicable
• Allocation: RANDOMIZED
• Masking: NONE
• Purpose: DIAGNOSTIC
• Intervention Model: PARALLEL
• Sponsor Type: OTHER
• Responsible Party: PRINCIPAL INVESTIGATOR
• PI Title: principle investigator

Study Record Dates

• First Submitted: September 17, 2023
• First Posted: September 22, 2023
• Study Start: September 30, 2023
• Primary Completion: September 30, 2024
• Study Completion: September 30, 2024
• Last Updated: January 23, 2026

Record last verified: 2026-01

Locations

EG (1)