Tregs CD25 CXCL9 in Vitiligo

NCT ID: NCT05569096

Last Updated: 2022-10-06

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

NOT_YET_RECRUITING

Total Enrollment

40 participants

Study Classification

OBSERVATIONAL

Study Start Date

2024-01-31

Study Completion Date

2026-01-31

Brief Summary

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Clinical significance of circulating T regulatory cells , soluble CD25 and CXCL9 to assess disease activity of vitiligo.

Detailed Description

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Vitiligo is an acquired and polygenic skin depigmenting disease characterized by bilateral, symmetrical depigmented patches over the entire body.

Its pathogenesis is multifactorial; however, the exact mechanisms that integrate the individual genetic susceptibility, melanocyte auto aggression, and failure of immune tolerance mechanisms are still not fully understood. The presence of these autoreactive CD8+ and CD4+ T cells in vitiligo patients' skin and blood samples . indicates a dysregulation of regulatory T-cell mechanism, which can suppress these cells.

Previous studies have reported an altered Treg cell frequency and function in vitiligo patients.

FoxP3 is the key transcriptional regulators of Tregs which mediate Treg cell function by repressing the expression of cytokines (IL2 and IL4 ) and upregulate the Treg cell markers (CTLA-4 and CD25 ).

Expression of IL-2 and its receptor CD25 are the most fundamental events in the host immune response. Thus any disorder in which T lymphocyte activation occurs at a substantial level is expected to induce expression of CD25 beyond ambient levels; this had been reported in atopic asthma, multiple sclerosis, allergic responses.

CD4+ CD25 FoxP3+ Tregs are important in maintaining self-tolerance and regulating immune responses in both physiological and pathological conditions .

Chemokines are important inflammatory factors that participate in many autoimmune responses.

C-X-C motif chemokine ligand 9 (CXCL9) is linked to the Th1 pattern and has been suggested as one of the most relevant chemokine axes that promote T-cell migration in different autoimmune and inflammatory processes.

In vitiligo, CXCL9 has been suggested to promote melanocyte-specic CTLs to in ltrate into the basal layer of the epidermis to attack melanocytes, resulting in the deficiency of melanin.

Conditions

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Vitiligo CD25 Deficiency Chemokine (C-X-C Motif) Tregs

Study Design

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Observational Model Type

CASE_CONTROL

Study Time Perspective

RETROSPECTIVE

Interventions

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ELIZA , Flowcytometry

CD25 , CXCL9 by ELISA. T cell population , T regulatory cells by Flow cytometry.

Intervention Type DIAGNOSTIC_TEST

Eligibility Criteria

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Inclusion Criteria

* Non segmental vitiligo.

Exclusion Criteria

The following patients were excluded from this study:

* Patients receiving systemic treatment in the last two months.
* Patients with any autoimmune disease, such as rheumatoid arthritis. inflammatory bowel disease, psoriasis, or systemic lupus erythematosus; patients with type 1 diabetes mellitus.
* Patients with any thyroid and/or neoplastic diseases.
Minimum Eligible Age

15 Years

Maximum Eligible Age

65 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

No

Sponsors

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Assiut University

OTHER

Sponsor Role lead

Responsible Party

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Jian Hashim Mohammed , MD

Assistant Lecturer

Responsibility Role PRINCIPAL_INVESTIGATOR

Central Contacts

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jian hashim, Assistant lecturer

Role: CONTACT

01061545086

Tarek Taha, Assistant professor

Role: CONTACT

01095472946

References

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Gharib K, Gadallah H, Elsayed A. Chemokines in Vitiligo Pathogenesis: CXCL10 and 12. J Clin Aesthet Dermatol. 2021 Sep;14(9):27-32.

Reference Type BACKGROUND
PMID: 34980968 (View on PubMed)

Marchioro HZ, Silva de Castro CC, Fava VM, Sakiyama PH, Dellatorre G, Miot HA. Update on the pathogenesis of vitiligo. An Bras Dermatol. 2022 Jul-Aug;97(4):478-490. doi: 10.1016/j.abd.2021.09.008. Epub 2022 May 25.

Reference Type BACKGROUND
PMID: 35643735 (View on PubMed)

Bergqvist C, Ezzedine K. Vitiligo: A Review. Dermatology. 2020;236(6):571-592. doi: 10.1159/000506103. Epub 2020 Mar 10.

Reference Type BACKGROUND
PMID: 32155629 (View on PubMed)

Giri PS, Dwivedi M, Laddha NC, Begum R, Bharti AH. Altered expression of nuclear factor of activated T cells, forkhead box P3, and immune-suppressive genes in regulatory T cells of generalized vitiligo patients. Pigment Cell Melanoma Res. 2020 Jul;33(4):566-578. doi: 10.1111/pcmr.12862. Epub 2020 Jan 23.

Reference Type BACKGROUND
PMID: 31917889 (View on PubMed)

Yang L, Yang S, Lei J, Hu W, Chen R, Lin F, Xu AE. Role of chemokines and the corresponding receptors in vitiligo: A pilot study. J Dermatol. 2018 Jan;45(1):31-38. doi: 10.1111/1346-8138.14004. Epub 2017 Nov 8.

Reference Type BACKGROUND
PMID: 29115683 (View on PubMed)

Yang L, Wei Y, Sun Y, Shi W, Yang J, Zhu L, Li M. Interferon-gamma Inhibits Melanogenesis and Induces Apoptosis in Melanocytes: A Pivotal Role of CD8+ Cytotoxic T Lymphocytes in Vitiligo. Acta Derm Venereol. 2015 Jul;95(6):664-70. doi: 10.2340/00015555-2080.

Reference Type BACKGROUND
PMID: 25721262 (View on PubMed)

Other Identifiers

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Tregs CD25 CXCL9 vitiligo

Identifier Type: -

Identifier Source: org_study_id

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