CD4+ T Cells and S100A7 Epression in Normal and Psoriatic Skin: A Histological and Histochemical Study
NCT ID: NCT06050330
Last Updated: 2026-01-23
Study Results
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Basic Information
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COMPLETED
NA
40 participants
INTERVENTIONAL
2023-09-30
2024-09-30
Brief Summary
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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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Detailed Description
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Conditions
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Study Design
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RANDOMIZED
PARALLEL
DIAGNOSTIC
NONE
Study Groups
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cases group
patients with psoriasis
skin biopsy
Paraffin sections,5 Um thick will be prepared from the skin samples and will be analyzed for light microscopy
control group
Healthy
skin biopsy
Paraffin sections,5 Um thick will be prepared from the skin samples and will be analyzed for light microscopy
Interventions
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skin biopsy
Paraffin sections,5 Um thick will be prepared from the skin samples and will be analyzed for light microscopy
Eligibility Criteria
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Inclusion Criteria
Exclusion Criteria
2. lactation
ALL
No
Sponsors
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Sohag University
OTHER
Responsible Party
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Ashrakat Abdelhamid Amin
principle investigator
Locations
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Sohag university Hospital
Sohag, , Egypt
Countries
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References
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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.
Lowes MA, Suarez-Farinas M, Krueger JG. Immunology of psoriasis. Annu Rev Immunol. 2014;32:227-55. doi: 10.1146/annurev-immunol-032713-120225.
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.
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.
Other Identifiers
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soh-Med-23-09-01MS
Identifier Type: -
Identifier Source: org_study_id
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